Aspen Neuroscience: DRS filing (amended)

Cover page 4 changes

As confidentially submitted to the Securities and Exchange Commission on March 30, May 12, 2026. This draft registration statement has not been publicly filed with the Securities and Exchange Commission and all information herein remains strictly confidential.

19 unchanged paragraphs

Aspen Neuroscience, Inc.

10835 Road to the Cure, Suite 100

19 unchanged paragraphs

Investing in our common stock involves a high degree of risk. See section titled Risk Factors beginning on page 14 15 to read about factors you should consider before deciding to invest in shares of our common stock.

21 unchanged paragraphs

Prospectus summary 18 changes

This summary highlights selected information contained elsewhere in this prospectus and is qualified in its entirety by the more detailed information and financial statements included elsewhere in this prospectus. This summary does not contain all of the information you should consider before investing in our common stock. You should carefully read this entire prospectus, including the information in the sections titled Risk Factors, Management s Discussion and Analysis of Financial Condition and Results of Operations and Special Note Regarding Forward-Looking Statements, and our financial statements and related notes included elsewhere in this prospectus, before making an investment decision. Unless the context requires otherwise, references in this prospectus to Aspen, the Company, we, us, and our refer to Aspen Neuroscience, Inc. Overview Aspen Neuroscience, Inc. is a leading, clinical-stage regenerative medicine biotechnology company focused on developing autologous induced-pluripotent stem cell (iPSC)-derived therapies to address neurodegenerative diseases with high unmet medical need. Our lead product, sasineprocel, is an investigational single-dose, autologous iPSC-based cell therapy being evaluated for the treatment of Parkinson s disease (PD). We believe sasineprocel has the potential to be disease-modifying by primarily replacing a patient s lost dopaminergic (DA) neurons with dopaminergic neuron precursor cells (DANPCs). In an ongoing Phase 1/2a ASPIRO clinical trial of sasineprocel in mid-stage to moderately advanced sporadic PD, patients have experienced, what we believe to be, sustained and clinically meaningful improvements in both motor, quality of life, and non-motor symptoms as measured by comparison to clinically meaningful change benchmarks. Based on these data, findings, we believe sasineprocel has the potential to improve upon the current standard of care in PD and address the significant unmet need in PD for a disease-modifying therapy that may slow or halt the progression of this devastating disease.

3 unchanged paragraphs

Sasineprocel and our end-to-end autologous iPSC platform are underpinned by Nobel Prize winning discoveries based on advances in cellular reprogramming, including the Nobel Prize winning discovery by Shinya Yamanaka and John B. Gurdon, which demonstrated that mature, specialized cells can be reprogrammed into pluripotent stem cells (iPSCs) through the introduction of defined transcription factors (commonly referred to as Yamanaka factors). We combine these foundational reprogramming methods with our stem cell biology expertise, the latest artificial intelligence, machine learning (ML) and genomic approaches to optimize cell identity, purity and functional potential and to enable a scalable, reproducible, standardized, and data-driven manufacturing process for autologous cell therapy. Sasineprocel, our proprietary autologous iPSC-derived composition of DANPCs, CNS progenitors, and glial progenitors, is designed to establish a biologically active cellular microenvironment that supports cell engraftment, survival, and functional integration of transplanted cells with the goal of restoring functional dopamine signaling in PD patients. We believe the sustained benefit that has been observed in certain patients treated with sasineprocel provides evidence of neural circuity circuitry reconstruction and is further supported by preclinical studies, in which we observed that DANPCs transplanted into PD animal models differentiated into DA neurons that integrated into the brain and restored dopamine signaling. We hypothesize that sasineprocel s combination of cells beyond DANPCs may play a key role in supporting neural synapse formation and general microenvironmental health to enable a broad and profound treatment effect in PD patients, including improvement in non-motor symptoms.

1 unchanged paragraph

We are developing sasineprocel, a single-dose, autologous iPSC-based therapeutic candidate for PD that is designed to replace a patient s lost dopamine neurons. We are currently conducting the open-label Phase 1/2a ASPIRO trial of a single dose of sasineprocel in mid-stage to moderately advanced PD patients. The trial consists of four cohorts at two dose levels, both of which were anticipated to be biologically active and have pharmacologic effects based on our preclinical modeling, with sasineprocel administered as a single bilateral intracranial injection into the post-commissural putamen using well-understood, standard stereotactic neurosurgical techniques.

As of February 24, April 7, 2026, the data cutoff date, 14 15 patients had been dosed, with six seven participants receiving a low dose and eight participants receiving a high dose. Sasineprocel was observed to be generally well-tolerated with the majority of reported adverse events being mild to moderate. Among the patients dosed, 58 treatment-emergent adverse events (TEAEs) were reported. There was no evidence of graft-induced dyskinesias or graft rejection, and no clinically significant hemorrhages were observed post-operatively. As sasineprocel is autologous, with no treatment-related adverse requirement for immunosuppression, there were no immunosuppression-related events. Only one TEAE was considered possibly related to sasineprocel. observed in the study, other than One that was possibly participant had two serious adverse events related to the surgical procedure. The most commonly reported TEAEs, defined as occurring in 10% or more of patients, were related to the surgery. See Business Lead Program: Sasineprocel for PD for additional information regarding the safety profile observed in the ASPIRO trial. As of the data cutoff date, 12 patients had at least one six-month or later follow up evaluation.

We assessed clinical efficacy outcomes every six months after administration of sasineprocel. We observed improvements across several secondary and exploratory endpoints, including changes in Good On time, Movement Disorder Society Sponsored Revision of the Unified Parkinson's Parkinson s Disease Rating Scale (MDS-UPDRS) Part III OFF. Consistent with these motor improvements, we also observed improvements in activities of daily living and quality of life measures assessed by MDS-UPDRS Part II ON, and Parkinson s Disease Questionnaire (PDQ-39) scores, as summarized below. Certain of the secondary endpoints used in this trial, including Good On Time and MDS-UPDRS Part III OFF, are validated registrational endpoints used in previous PD registrational clinical trials. Each of these outcomes The mean improvements at 12 18 months for Good On Time and MDS-UPDRS Part III OFF scores in both cohorts as well as 18 months for the low dose cohort, were above clinically meaningful change benchmarks. which we estimated based The mean PDQ-39 and MDS-UPDRS Part II ON published literature. scores improved above clinically meaningful change benchmarks in the low dose cohort and were stable in the high dose cohort at 18 months. Fluorodopa (FDOPA) positron emission tomography (PET) imaging is also being used to evaluate the engraftment of cells. FDOPA PET imaging showed elevated FDOPA uptake values at 6, 12, and 18 months following sasineprocel administration compared to baseline, which is evidence of the survival, viability, and integration of transplanted iPSCs. Clinically meaningful change benchmarks are reviewed on an ongoing basis during the trial and reflect management s belief based on a review of published literature, regulatory agency guidelines and precedent in PD clinical research, and discussions with key opinion leaders in the field. The benchmarks have not been discussed with the FDA or any other government regulatory authority, and have not been independently validated by any third parties.

Additionally, the ASPIRO trial is exploring changes in DA medication as measured by levodopa equivalent daily dose (LEDD). As of the LEDD cutoff date of March 24, April 10, 2026, in the low dose cohort, two, three and four patients showed a reduction in LEDD at six, 12 and 18 months, respectively, and no patients experienced an LEDD increase. In the high dose cohort, at six months, three out of eight patients showed an LEDD reduction and one patient showed an LEDD increase; at 12 months, two out of four patients showed an LEDD reduction and one patient showed an LEDD increase; at 18 months, three out of four patients showed an LEDD reduction and one showed an LEDD increase.

Figure 1. Sustained clinically meaningful improvements observed across multiple validated PD endpoints. Data summarized above is as of February 24, April 7, 2026, except LEDD data is summarized as of March 24, April 10, 2026. A decrease (negative number) compared to baseline is an improvement for MDS-UPDRS scores and PDQ-39. The numbers in parentheses represent standard deviations. * *For the four high dose patients for whom data was available at the 12-month assessment, and 18-month assessments, the baseline values for Good On Time (hrs) (hours) Hauser Diary, Off Time (hours) Hauser Diary, MDS-UPDRS part III OFF score, MDS-UPDRS part II score, and PDQ-39 were: 11.7 (0.9), 4.3 (0.9), 44.0 (4.2), 9.5 (9.3), 16.1 (15.6), respectively. For the three low dose patients in Cohort 4, no data is yet available because six months have not elapsed since dosing.

The Phase 1/2a ASPIRO trial is an open-label trial and does not include a placebo or control cohort. Open-label trials are subject to inherent limitations that may affect the interpretation of clinical results and may not be predictive of future clinical trial results when studied in a controlled environment with a placebo or active control. See Risk Factors Risks Related to the Discovery, Development, and Regulatory Approval of Our Product Candidates for additional information regarding the limitations of our clinical trial design.

Sasineprocel has received Fast Track designation from the U.S. Food and Drug Administration (FDA) for the treatment of PD to improve motor function. Fast Track designation does not ensure a faster development or regulatory review or approval process and does not increase the likelihood that sasineprocel will receive regulatory approval. We anticipate that sasineprocel would be regulated as a combination product by the FDA because it is designed to be administered through drug delivery devices. See the section titled Risk Factors Fast Track designation by the FDA for sasineprocel, and other expedited designations if granted in the future, may not lead to a faster development or regulatory review or approval process, and do not increase the likelihood that sasineprocel or any other product candidate which may receive such designations will receive regulatory approval for more information. We expect to report further long-term data from the ASPIRO trial in . We have begun enrolling patients and are preparing to initiate dosing a new cohort in the Phase 1/2a ASPIRO trial to evaluate sasineprocel in patients with genetic PD. We anticipate initiating biopsy collection for the Phase 3 trial in . Following feedback from the FDA, and additional data from the ASPIRO trial, if positive, we anticipate initiating a dosing patients in the Phase 3 trial in . In addition, we plan to dose up to 12 approximately six patients with genetic PD in the ASPIRO trial. Pending results from this cohort, we intend to include all patients with PD (including both sporadic and genetic PD) in our Phase 3 program.

2 unchanged paragraphs

We have developed an integrated, end-to-end autologous iPSC platform (our platform) designed to generate patient-specific cell therapies for neurodegenerative diseases. Our platform combines proprietary cell reprogramming methods, automated and scalable manufacturing processes, and comprehensive quality control (QC) systems, including advanced genomics and bioinformatics, to produce DANPCs with consistent identify, identity, purity, and functional characteristics.

To manufacture sasineprocel, dermal fibroblast cells are generated from a PD patient via a minimally invasive skin biopsy (3mm), expanded, and reprogrammed into iPSCs using defined transcription factors (Yamanaka factors). These iPSCs undergo rigorous characterization to confirm sterility, identity, purity and pluripotency, and are subsequently differentiated into DANPCs using our proprietary processes. The final product consists primarily of DANPCs with defined levels of supporting neural progenitor cell types, and is cryopreserved and released based on established specifications for cell concentration, purity, identity, and potency before shipment for patient administration. We are reliant on a number of licenses from third parties for our manufacturing platform, as it relates to sasineprocel, including from iPS Academia Japan, Inc. and Sumitomo Pharma Co. Ltd. for transcription factors and reprogramming methods, the Scripps Research Institute for a specific cell characterization assay, and Cell X technologies for automation. See Business Licensing and Collaboration Agreements for additional information.

Our platform is designed to address key challenges associated with autologous cell therapies, including inter-patient variability, genomic instability, and inconsistent differentiation. To mitigate these risks, we utilize multiple orthogonal assays and proprietary reference datasets to assess genetic identity, genomic integrity, lineage specification, purity, and functional attributes prior to clinical use. Building on foundational work from our scientific founders, we have established rigorous product release criteria supported by these datasets to enable consistent product characterization, including DANPC identity, maturity, engraftment potential and dopamine release, complemented by in vitro bioassays assessing cellular functionality and post-cryopreservation stability. In parallel, we are developing an automated, robust, modular manufacturing framework designed to streamline and standardize production, reduce manual variability and support scalable, reproducible manufacturing with the capacity to treat hundreds of patients annually. This modular automation template has a small cleanroom footprint (approximately 5,000 square feet) and is intended to be replicated and scaled up to meet future patient demand. The production process is performed in three stages. Stage 1 (skin to fibroblast) has a manufacturing duration of approximately three weeks. Stage 2 (fibroblasts to iPSCs) has a duration of approximately eight weeks. Stage 3 (iPSCs to DANPCs) has a duration of approximately five weeks. Following each stage, we complete QC testing which typically takes a total of four to five weeks. However, following Stage 1 and Stage 2, we perform initial QC testing to conditionally release the fibroblasts and iPSCs to the next stage, which typically takes one to two weeks, before completing the full QC testing process.

1 unchanged paragraph

We have assembled a management team and scientific organization with substantial experience across neuroscience research, drug discovery and development, regulatory strategy, commercialization and manufacturing. Aspen Neuroscience was founded in 2018 based on more than two decades of research conducted by Jeanne F. Loring, Ph.D., Professor Emeritus Emerita at the Scripps Research Institute and founding Director of the Center for Regenerative Medicine. Dr. Loring s laboratory developed foundational methods for reprogramming adult human cells into iPSCs and subsequently differentiating them into dopamine-producing neurons, which form the basis of our autologous iPSC platform and sasineprocel. Since inception, we have focused on translating this academic innovation into a clinically scalable, regulatory-compliant therapeutics platform.

32 unchanged paragraphs

We were incorporated in Delaware in on May 18, 2018, under the name Aspen Biosciences, Inc. and changed our name to Aspen Neuroscience, Inc. in October 2018. Our principal executive offices are located at 10835 Road to the Cure, Suite 100, San Diego, CA, 92121. Our telephone number is (858) 263-1222. Our website address is www.aspenneuroscience.com . Information contained on our website is not incorporated by reference into this prospectus, and it should not be considered to be part of this prospectus.

15 unchanged paragraphs

We estimate that the net proceeds to us from this offering will be approximately $ million (or approximately $ million if the underwriters exercise their option to purchase additional shares of our common stock in full) from the sale of the shares of common stock offered by us in this offering, based on an assumed an initial public offering price of $ per share, which is the midpoint of the price range set forth on the cover page of this prospectus, and after deducting the estimated underwriting discounts and commissions and estimated offering expenses payable by us.

We currently intend to use the net proceeds from this offering, together with our existing cash, cash equivalents and marketable securities, to fund the clinical development of sasineprocel, to fund the development of including the ongoing Phase 1/2a ASPIRO trial and the initiation of a Phase 3 trial in sporadic and genetic PD, to fund the research and development of our other product candidates and for working capital and general corporate purposes. See the section titled Use of Proceeds for additional information.

24 unchanged paragraphs

Weighted-average shares used in net loss per common share calculation, basic and diluted (1) 10,318,638 9,261,740 Pro forma net loss per common share, basic and diluted (unaudited) (2) $ (0.48 ) $ (0.44 ) Pro forma weighted-average shares used in pro forma net loss per common share calculation, basic and diluted (unaudited) (2) 129,963,415 110,682,104 (1) See Note 12 to our audited financial statements included elsewhere in this prospectus for an explanation of the methods used to calculate historical net loss per share, basic and diluted, and the weighted-average number of shares of common stock used in the computation of the per share amounts.

(2) Unaudited pro forma net loss per share, basic and diluted, attributable to common stockholders, is calculated giving effect to the conversion of all outstanding shares of our convertible preferred stock into shares of our common stock. Unaudited pro forma net loss per share attributable to common stockholders does not include the shares expected to be sold and related proceeds to be received in this offering. Unaudited pro forma net loss per share attributable to common stockholders for the years year ended December 31, 2025 and 2024 were was calculated using the weighted-average number of shares of common stock outstanding, including the pro forma effect of the conversion of all outstanding shares of our convertible preferred stock into shares of our common stock, as if such conversion had occurred at the beginning of the period, or their issuance dates.

8 unchanged paragraphs

Risk factors 9 changes

19 unchanged paragraphs

Based on our current operating plans, we believe that the net proceeds from this offering, together with our existing cash, cash equivalents and marketable securities, will be sufficient to fund our operations into . In particular, we expect that the net proceeds from this offering and our existing cash, cash equivalents and marketable securities will allow us to continue to fund the Phase 1/2a ASPIRO trial evaluating sasineprocel in patients with sporadic and genetic PD, to continue to fund the development of sasineprocel in PD patients, including initiating a Phase 3 trial, and to continue to fund the development of our microglia program through the initiation of IND-enabling studies, and the remainder for working capital and other general purposes. We have based these estimates on assumptions that may prove to be wrong, and we could use our capital resources sooner than we currently expect. Our operating plans and other demands on our cash resources may change as a result of many factors currently unknown to us, and we may need to seek additional funds sooner than planned. The net proceeds of this offering, together with our existing cash, cash equivalents and marketable securities, will not be sufficient to complete the Phase 1/2a ASPIRO trial, the Phase 3 trial for sasineprocel, or the development of sasineprocel or any other current or future product candidates. and After this offering, we will require additional capital in order to advance our current and future product candidates through clinical trials, regulatory approval, and commercialization. Accordingly, we will need to obtain substantial additional funding in connection with our continuing operations. Our ability to raise additional funds may be adversely impacted by global economic conditions, disruptions to, and volatility in, the credit and financial markets in the United States and worldwide, and diminished liquidity and credit availability. If the equity and credit markets deteriorate, it may make any necessary debt or equity financing more difficult, more costly, and more dilutive. If we are unable to raise capital when needed or on attractive terms, we could be forced to delay, reduce, or eliminate our research and development programs or any future commercialization efforts, or even cease operations. We expect to finance our cash needs through public or private equity or debt financings or other capital sources, including potential collaborations, licenses, royalty financing and other similar arrangements. In addition, we may seek additional capital due to favorable market conditions or strategic considerations even if we believe we have sufficient funds for our current or future operating plans. Attempting to secure additional financing may divert our management from our day-to-day activities, which may adversely affect our ability to develop our product candidates.

37 unchanged paragraphs

Additionally, our ongoing Phase 1/2a ASPIRO trial is an open-label trial and does not include a placebo or control cohort. The results of the ASPIRO trial or any other open-label trial that we may conduct may not be predictive of future clinical trial results when studied in a controlled environment with a placebo or active control. An open-label clinical trial is one where both the patient and investigator know whether the patient is receiving the investigational product candidate or either an existing approved drug or placebo. Open-label clinical trials are subject to various limitations that may exaggerate any observed therapeutic effect as patients in open-label clinical trials are aware that they are receiving an experimental treatment. Open-label clinical trials may be subject to a patient bias where patients perceive their symptoms to have improved merely due to their awareness of receiving an experimental treatment. In addition, open-label clinical trials may be subject to an investigator bias where those assessing and reviewing the physiological outcomes of the clinical trials are aware of which patients have received treatment and may interpret the information of the treated group more favorably given this knowledge. If the limitations of our open-label clinical trial design cause us to overestimate the therapeutic effects of sasineprocel, we may experience setbacks in later-stage clinical development, which could delay or prevent regulatory approval. We expect to include a control group in our planned Phase 3 trial. However, even if we observe positive results in a controlled Phase 3 trial, there can be no assurance that such results will be sufficient to obtain regulatory approval.

61 unchanged paragraphs

we may be subject to fines or criminal or civil penalties;

8 unchanged paragraphs

We are currently conducting the open-label Phase 1/2a ASPIRO trial of single dose of sasineprocel in PD patients, and plan to advance sasineprocel into a Phase 3 trial following feedback from the FDA. and additional data from the ASPIRO trial. We have not yet completed any later-stage or pivotal clinical trials for sasineprocel or any other product candidate. Carrying out later-stage clinical trials and the submission of a successful BLA or other comparable foreign regulatory submission is a complicated process. We also have limited experience as a company in preparing and submitting marketing applications and have not previously submitted a BLA or other comparable foreign regulatory submission for any product candidate. In addition, we have had limited interactions with the FDA and cannot be certain how many additional clinical trials of sasineprocel or any other product candidate will be required or how such additional trials should be designed. Consequently, we may be unable to successfully and efficiently execute and complete necessary clinical trials in a way that leads to submission of a BLA and regulatory approval of any of our product candidates. We may require more time and incur greater costs than our competitors and may not succeed in obtaining regulatory approvals of product candidates that we develop. Failure to commence or complete, or delays in, our ongoing or planned clinical trials could prevent us from or delay us in submitting BLAs or other comparable foreign regulatory submissions for and commercializing our product candidates.

1 unchanged paragraph

We are developing certain of our product candidates, including sasineprocel, to be administered through drug delivery devices. Accordingly, we anticipate expect that sasineprocel would will be regulated as a combination product by the FDA and other regulatory authorities. Combination products require coordination within the FDA and within comparable regulatory agencies for review of their the biologic product and device components. For example, the FDA s review of a marketing application for sasineprocel may include the participation of both the FDA s Center for Biologics Evaluation and Research and the FDA s Center for Devices and Radiological Health. Although the FDA and comparable foreign agencies have or may have systems in place for the review and approval of combination products, we may experience additional delays in the development and commercialization of such product candidates due to regulatory timing constraints and uncertainties in the product development and approval process. Moreover, although we anticipate that the device component of any combination product candidates we develop will be reviewed within the usual time frames expected for the underlying biologic component application, and that no separate marketing application for the device components of such product candidates will be required in the United States, the FDA or comparable regulatory authorities may delay approval or require us to conduct additional studies with the device which may delay the approval of the combination product.

6 unchanged paragraphs

Prior to obtaining approval to commercialize a product candidate in the United States or abroad, we must demonstrate with substantial evidence from adequate and well-controlled clinical trials, and to the satisfaction of the FDA or comparable foreign regulatory authorities, that such product candidates are safe and effective for their intended uses, and in the case of biological products in the United States, that such product candidates are safe, pure and potent for their intended uses. Results from nonclinical studies and clinical trials can be interpreted in different ways. Even if we believe available nonclinical or clinical data support the safety, purity, and potency (or efficacy) of our product candidates, such data may not be sufficient to obtain approval from the FDA and comparable foreign regulatory authorities. The FDA or comparable foreign regulatory authorities, as the case may be, may also require us to conduct additional preclinical studies or clinical trials for our product candidates either. The FDA or comparable foreign regulatory authorities can delay, limit or deny approval of a product candidate for many reasons, including:

The FDA or comparable foreign regulatory authorities can delay, limit or deny approval of a product candidate for many reasons, including:

189 unchanged paragraphs

As of January March 31, 2026, we had 117 full-time employees and three part-time employees. As we continue development and pursue the potential commercialization of our product candidates, as well as transition to functioning as a public company, we will need to expand our financial, development, regulatory, manufacturing, information technology, marketing, and sales capabilities or contract with third parties to provide these capabilities for us. As our operations expand, we expect that we will need to manage additional relationships with various strategic partners, suppliers, and other third parties, and we may not be successful in doing so. Our future financial performance and our ability to develop and commercialize our product candidates and to compete effectively will depend, in part, on our ability to manage any future growth effectively. Due to our limited financial resources and the limited experience of our management team in managing a company with such anticipated growth, we may not be able to effectively manage the expansion of our operations or recruit and train additional qualified personnel. The expansion of our operations may lead to significant costs and may divert our management and business development resources. Any inability to manage growth could delay the execution of our business plans or disrupt our operations.

14 unchanged paragraphs

In 2026, the U.S. government launched TrumpRx, a federal initiative to enable patients to gain access to certain prescription drugs at reduced costs based on pricing available in other countries (i.e., most-favored-nation pricing). In addition, the Trump administration is pursuing a two-fold strategy to reduce drug costs in the United States. While it is unclear whether and how the Trump proposals will be implemented, the Trump policies are likely to have a negative impact on the pharmaceutical industry and on our ability to receive adequate revenues for any product candidate that we commercialize. On the one hand, President Trump has threatened to impose significant tariffs on pharmaceutical manufacturers that do not adopt pricing policies such as most favored nation pricing, which would tie the price for drugs in the United States to the lowest price in a group of other countries. In response, multiple manufacturers have entered into confidential pricing agreements with the federal government. Subsequently, in April 2026, the Trump administration issued a proclamation imposing tariffs under Section 232 of the Trade Expansion Act on imports of brand pharmaceuticals, biologics and associated pharmaceutical ingredients, beginning July 31, 2026. Exempted from these tariffs, among others, are companies that have executed or are negotiating agreements with the federal government regarding most favored nation pricing and onshoring of production and research and development. On the other hand, the Trump administration is also pursuing traditional regulatory pathways to impose drug pricing policies and published two proposed regulations in December 2025, referred to as Globe and Guard. If finalized, these regulations would implement mandatory payment models under which manufacturers of eligible drugs would be required to pay rebates to the federal government on a portion of the units of their drugs that are reimbursed by Medicare, with the rebate amount based on most favored nation pricing. While the impact of the Globe and Guard proposed regulations, if finalized, cannot yet be determined, it is likely to be significant. Even regulatory proposals or executive actions that are ultimately deemed unlawful could negatively impact the U.S. pharmaceutical sector and our business.

226 unchanged paragraphs

Use of proceeds 3 changes

3 unchanged paragraphs

approximately $ million to continue funding the development of sasineprocel in PD patients, including initiating a Phase 3 trial;

approximately $ million to initiate and fund a Phase 3 trial evaluating sasineprocel in patients with sporadic and genetic PD;

3 unchanged paragraphs

The net proceeds from this offering, together with our existing cash, cash equivalents, and marketable securities will not be sufficient to complete the Phase 1/2a ASPIRO trial, the Phase 3 trial for sasineprocel, or the development of sasineprocel and or any other current or future product candidates. After this offering, we will require additional capital in order to advance our current and any future products through clinical trials, regulatory approval, and commercialization. Until such time, if ever, as we can generate substantial revenue, we expect to finance our cash needs through equity offerings, debt financings, or other capital sources, including potential collaborations, licenses, and other similar arrangements. Nevertheless, we may be unable to raise additional funds or enter into such other arrangements when needed on favorable terms or at all.

1 unchanged paragraph

Capitalization 1 change

9 unchanged paragraphs

The number of shares of our common stock issued and outstanding, pro forma and pro forma as adjusted in the table above, above is based on 188,208,087 shares of our common stock outstanding as December 31, 2025 after giving effect to the automatic conversion of all outstanding shares of our convertible preferred stock into 177,593,856 shares of our common stock immediately prior to the closing of this offering, and excludes:

4 unchanged paragraphs

MD&A 13 changes

35 unchanged paragraphs

Research and development expenses were $41.8 million for the years year ended December 31, 2025, compared to $35.6 million for the year ended December 31, 2024. The increase of $6.2 million was due to an increase in non-personnel costs primarily associated with the development and production of sasineprocel of $3.0 million, increased personnel costs for salaries, bonuses and benefits of $2.1 million, increased facilities costs of $0.5 million, increased depreciation expense of $0.4 million, and increased stock-based compensation expense of $0.2 million. Substantially all of our non-personnel research and development expenses for the years ended December 31, 2025 and 2024 related to our lead product candidate, sasineprocel. Non-personnel research and development expenses related to other programs were immaterial for the years ended December 31, 2025 and 2024.

47 unchanged paragraphs

During the normal course of our business, we enter into agreements with for research and professional services, and for the purchase of lab supplies used in our research and clinical trial activities. These agreements are important to our operations but do not involve material financial commitments and generally provide for termination after a notice period, and, therefore, are cancelable contracts and not separately presented. For more information regarding our operational relationships, see the section titled Business Manufacturing.

In March 2019, we entered into a lease agreement for office, research and development, and laboratory space located in San Diego, California, which commenced in April 2019. In June 2021, We subsequently amended the lease to expand the premises to approximately 31,000 rentable square feet and extend extended the term through September 15, 2027. We are required to maintain a letter of credit in the amount of $0.2 million as security for our obligations under this lease, which is recorded as restricted cash.

In May 2021, we entered into a lease agreement for approximately 22,000 rentable square feet of office, research and development, and laboratory, GMP manufacturing and warehouse space located in La Jolla, San Diego, California. This lease commenced on April 1, 2022, and has a term expiring on July 31, 2032, with one option to renew for an additional five-year term. We are required to maintain a letter of credit in the amount of $0.4 million as security for our obligations under this lease, which is recorded as restricted cash.

As of December 31, 2025, total future minimum lease payments under our operating lease agreements was were $13.4 million.

1 unchanged paragraph

In October 2018, we were assigned an exclusive license agreement by Summit for Stem Cell Foundation with the Scripps Research Institute (TSRI) under which we acquired the exclusive license to intellectual property, which allows us to substantially facilitate the development of the licensed intellectual property (the TSRI License Agreement). The TSRI License Agreement includes the payment of royalties equal to a low single digit percentage on future net sales of licensed products. If we sublicense a product under the TSRI License Agreement, we are obligated to pay TSRI a mid-single-digit percentage of non-royalty sublicensing consideration. Payments related to the TSRI License Agreement are made in the period when the contingency is resolved, and the amounts become payable. No amounts have been payable under this agreement.

In October 2018, we were assigned an exclusive license agreement effective July 2018 by Summit for Stem Cell Foundation with the Scripps Research Institute ( TSRI , and the agreement, the TSRI License Agreement ). Under the TSRI License Agreement, TSRI granted us an exclusive, worldwide, royalty-bearing license, with the right to sublicense through multiple tiers (subject to certain conditions), under certain intellectual property relating to certain methods for differentiating DA neurons from iPSCs and certain bioinformatics assays, and together with certain licensed biological materials, to make, have made, use, have used, sell, have sold, offer for sale and import licensed products, services and processes in all fields worldwide. The licensed intellectual property includes methods that are used in the manufacture of sasineprocel. TSRI reserved rights in the licensed intellectual property and/or licensed biological materials for non-corporate sponsored internal research and educational purposes without obligation to further compensate us for such uses and further reserved the right to grant similar non-exclusive licenses to other nonprofit or academic institutions for similar internal research and educational purposes.

Under the TSRI License Agreement, we are obligated to use commercially reasonable efforts to develop and obtain regulatory approval for, and, if applicable, market and sell licensed products, services and processes in sufficient quantities to meet market demands. In addition, for each of the disclosed inventions and intellectual property described above that are the subject of our license, we are obligated to achieve certain development diligence benchmarks relating to intellectual property development and regulatory filings by specified anniversaries of the TSRI License Agreement s effective date. Such benchmarks may be extended by us up to two times for a certain number of months upon the payment of a fee. If we fail to achieve such development diligence benchmarks, TSRI has the right, at its option, to either terminate the TSRI License Agreement in its entirety, terminate our rights with respect to specific licensed products, services or processes, or convert the license granted to us to non-exclusive upon advance notice.

We paid TSRI a non-creditable, non-refundable license issue upfront fee of $1,000. We are further obligated to pay TSRI a running royalty of 1.0% on future net sales of licensed products, services and processes on a licensed product-by-licensed product and country-by-country basis. We are also obligated to pay TSRI the following percentage of non-royalty sublicensing revenues: (a) 15% if the sublicense is executed prior to the third anniversary of the effective date of the TSRI License Agreement, and (b) 5% if executed thereafter. Sublicense revenue fees paid by us in the first year after execution of the applicable sublicense shall be capped at $250,000. Payments related to the TSRI License Agreement are made in the period when the contingency is resolved, and the amounts become payable. Other than the non-creditable, non-refundable license issue upfront fee, no amounts have been payable under the TSRI License Agreement.

Unless terminated earlier, the TSRI License Agreement expires upon such time as no further royalties are due to TSRI, which lasts, on a country-by-country basis, until ten years after the date of first commercial sale of the first licensed product, licensed process, or licensed service sold in such country that was covered by the same invention disclosure among the disclosed intellectual property, but in any event no later than 20 years following the effective date of the TSRI License Agreement. We may terminate the TSRI License Agreement for convenience at any time upon advance notice to TSRI. TSRI may terminate the TSRI License Agreement for our material breach (subject to separate cure periods depending on whether our breach is payment-related or not), certain insolvency proceedings involving us, or if we commit a felony relating to the development, manufacture, use, marketing, distribution or sale of licensed products, services, processes or biological materials. Upon any early termination, the licenses granted to us terminate and such rights revert to TSRI.

1 unchanged paragraph

In September 2019, we entered into a non-exclusive license agreement with iPS Academia Japan, Inc. (the AJ License Agreement) pursuant to which iPS Academia Japan, Inc. (AJ) granted us a license under the licensed patents for the development, manufacture, and sale of licensed products. Pursuant to the AJ License Agreement, we are obligated to pay AJ an upfront fee of $60,000 and annual maintenance fees of $25,000 until and including the calendar year in which we obtain approval of a first new drug application of a licensed product. We are obligated to pay future milestone payments up to $0.7 million $135,000 upon the successful achievement of developmental milestones, and up to $1.1 million when certain net sales thresholds of a licensed product are met. We are obligated to pay future royalty payments in the low single digit percentage of net sales of licensed products. We will also be subject to an annual minimum royalty of $25,000 following the first approval of a licensed product. We recognize the expense of the milestones when payable.

5 unchanged paragraphs

In January 2024, we entered into a Secured Convertible Promissory Note Purchase Agreement with Cell X (Cell X Convertible Note Purchase Agreement) whereby we agreed to purchase, and Cell X agreed to sell and issue, a convertible promissory note (Cell X Convertible Note) with an original principal amount equal to $5.0 million and 8% interest rate. The outstanding amount shall automatically convert into shares of Cell X s preferred stock (the Conversion Stock) upon a qualified financing and have optional conversion upon a non-qualified equity financing. The principal and accrued interest are due and payable upon the earliest to occur of (i) the 24-month anniversary of the Cell X Convertible Note Purchase Agreement, (ii) a change in control of Cell X or (iii) the occurrence of an event of default, as defined in the Cell X Convertible Note Purchase Agreement. We purchased the $5.0 million note in 2024 and elected the fair value option for the note. The fair value of the Cell X Convertible Note was $0.9 million and $5.5 million as of December 31, 2025 and December 31, 2024, respectively, which is included in other assets on the balance sheet. In January 2026, we amended the Cell X Convertible Note to extend the maturity date to February 2026, or such later date approved by us and Cell X. In February 2026, we extended the maturity date to March 2026, and in March 2026, we extended the maturity date to April 13, 2026. On April 10, 2026, we extended the maturity of the Cell X Convertible Note to April 30, 2026, and on April 29, 2026, we further extended the maturity to May 15, 2026.

We purchased the $5.0 million note in 2024 and elected the fair value option for the note. The fair value of the Cell X Convertible Note was $0.9 million and $5.5 million as of December 31, 2025 and December 31, 2024, respectively, which is included in other noncurrent assets on the balance sheet.

47 unchanged paragraphs

Business 84 changes

Aspen Neuroscience, Inc. is a leading, clinical-stage regenerative medicine biotechnology company focused on developing autologous iPSC-derived therapies to address neurodegenerative diseases with high unmet medical need. Our lead product, sasineprocel, is an investigational single-dose, autologous iPSC-based cell therapy being evaluated for the treatment of PD. We believe sasineprocel has the potential to be disease-modifying by replacing a patient s lost DA neurons with DANPCs, capable of integrating and reestablishing functional connections. In an ongoing Phase 1/2a ASPIRO clinical trial of sasineprocel in mid-stage to moderately advanced sporadic PD, patients have experienced, what we believe to be, sustained and clinically meaningful improvements in both motor, quality of life, and non-motor symptoms as measured by comparison to clinically meaningful change benchmarks. Based on these data, findings, we believe sasineprocel has the potential to improve upon the current standard of care in PD and address the significant unmet need for a disease-modifying therapy that may slow or halt the progression of this devastating disease. These benchmarks are reviewed on an ongoing basis during the trial and reflect management s belief based on a review of published literature, regulatory agency guidelines and precedent in PD clinical research, and discussions with key opinion leaders in the field. The benchmarks have not been discussed with the FDA or any other government regulatory authority, and have not been independently validated by any third parties.

3 unchanged paragraphs

As of February 24, 2026, the cutoff date, 14 patients had been dosed with six participants receiving a low dose and eight participants receiving a high dose. Sasineprocel was observed to be generally well-tolerated with the majority of reported adverse events being mild to moderate. The most common treatment-related adverse events were incision site pain, headache and swollen tongue, which were each related to the surgery. One patient experienced two serious adverse events related to the surgery. There were no treatment-related adverse events observed in the study. As of the cutoff date, 12 patients had at least one six-month follow up evaluation. We assessed clinical efficacy outcomes every six months after administration of sasineprocel. We observed improvements across several secondary and exploratory endpoints, including changes in Good On time, MDS-UPDRS Part III OFF, MDS-UPDRS Part II, and PDQ-39 scores, as summarized below. Certain of the secondary endpoints used in this trial are validated endpoints used in previous PD registrational clinical trials. Each of these outcomes at 12 months for both cohorts, as well as 18 months for the low dose cohort, were above clinically meaningful change benchmarks which we estimated based on the published literature. FDOPA PET imaging is also being used to evaluate the engraftment of cells.

Sasineprocel and our end-to-end autologous iPSC platform are underpinned by Nobel Prize winning discoveries based on advances in cellular reprogramming, including the Nobel Prize winning discovery by Shinya Yamanaka and John B. Gurdon, which demonstrated that mature, specialized cells can be reprogrammed into pluripotent stem cells (iPSCs) through the introduction of defined transcription factors (commonly referred to as Yamanaka factors). We combine these foundational reprogramming methods with our stem cell biology expertise, the latest artificial intelligence, ML and genomic approaches to optimize cell identity, purity and functional potential and to enable a scalable, reproducible, standardized, and data-driven manufacturing process for autologous cell therapy. Sasineprocel, our proprietary autologous iPSC-derived composition of DANPCs, CNS progenitors, and glial progenitors, is designed to establish a biologically active cellular microenvironment that supports cell engraftment, survival, and functional integration of transplanted cells with the goal of restoring functional dopamine signaling in PD patients. The sustained benefit observed in patients treated with sasineprocel provides evidence of neural circuity circuitry reconstruction and is further supported by preclinical studies, in which we observed that DANPCs transplanted into PD animal models differentiated into DA neurons that integrated into the brain and restored dopamine signaling. We hypothesize that sasineprocel s combination of cells beyond DANPCs may play a key role in supporting neural synapse formation and general microenvironmental health to enable a broad and profound treatment effect in PD patients, including improvement in non-motor symptoms.

We are currently conducting the open-label Phase 1/2a ASPIRO trial evaluating sasineprocel in patients with sporadic PD and have begun enrolling genetic PD patients. The trial consists of sequential dose cohorts with sasineprocel administered as a single bilateral intracranial injection into the post-commissural putamen, an area of the brain that participates in motor control, using well-understood, standard stereotactic neurosurgical techniques. The study s primary objective is to assess safety and tolerability. The study s secondary and exploratory objectives are to evaluate the potential efficacy of sasineprocel, measured by changes from baseline in multiple patient- and clinician-reported PD-specific outcomes. These include changes in MDS UPDRS Parts I-IV, which measures the severity and progression of PD, including motor and non-motor symptoms; Hauser diary (to measure Good On time, defined as time without troublesome dyskinesia); Non-Motor Symptoms Scale (NMSS); and quality of life measures including PDQ-39. FDOPA PET imaging is being used to evaluate the engraftment of cells. Certain of the secondary endpoints used in this trial are validated endpoints used in previous PD registrational clinical trials.

As of April 7, 2026, the data cutoff date, 15 patients had been dosed, with seven participants receiving a low dose and eight participants receiving a high dose. Sasineprocel was observed to be generally well-tolerated with the majority of reported adverse events being mild to moderate. Among the patients dosed, 58 treatment-emergent adverse events (TEAEs) were reported. There was no evidence of graft-induced dyskinesias or graft rejection, and no clinically significant hemorrhages were observed post-operatively. As sasineprocel is autologous, with no requirement for immunosuppression, there were no immunosuppression-related events. Only one TEAE, myoclonus (sudden, uncontrollable muscle movement), was considered possibly related to sasineprocel, with sertraline, a selective serotonin reuptake inhibitor, identified as a co-suspect medication. One participant had two serious adverse events related to the surgical procedure (neck swelling and dysphagia due to intubation in the prone position and stroke due to pre-operative interruption of anticoagulants that the patient was taking for a history of deep venous thrombosis). The most commonly reported TEAEs, defined as occurring in 10% or more of patients, were related to the surgery, including incision site pain, swollen tongue, headache, infusion site pain, glossodynia, hypoesthesia, and oropharyngeal pain. Two patients had intracranial hemorrhages not requiring any surgical treatment. Of these two patients, one patient had no associated symptoms and the other, who had a history of migraine, experienced a headache which resolved, with levetiracetam identified as a co-suspect medication. As of the data cutoff date, 12 patients had at least one six-month or later follow up evaluation.

We assessed clinical efficacy outcomes every six months after administration of sasineprocel. We observed improvements across several secondary and exploratory endpoints, including changes in Good On time (On time without troublesome dyskinesia normalized to 16 hours of the day), Off time, MDS-UPDRS Part III OFF, MDS-UPDRS Part II ON, and PDQ-39 scores, as summarized below. Certain of the secondary endpoints used in this trial, including Good On Time and MDS-UPDRS Part III OFF, are validated registrational endpoints used in previous PD registrational clinical trials. The mean improvements at 18 months for Good On Time and MDS-UPDRS Part III OFF scores in both cohorts were above clinically meaningful change benchmarks. The mean PDQ-39 and MDS-UPDRS Part II ON scores improved above clinically meaningful change benchmarks in the low dose cohort and were stable in the high dose cohort at 18 months. FDOPA PET imaging is also being used to evaluate the engraftment of cells. FDOPA PET imaging showed elevated FDOPA uptake values at 6, 12, and 18 months following sasineprocel administration compared to baseline, which is evidence of the survival, viability, and integration of transplanted iPSCs. Clinically meaningful change benchmarks are reviewed on an ongoing basis during the trial and reflect management s belief based on a review of published literature, regulatory agency guidelines and precedent in PD clinical research, and discussions with key opinion leaders in the field. The benchmarks have not been discussed with the FDA or any other government regulatory authority, and have not been independently validated by any third parties.

Additionally, the ASPIRO trial is exploring changes in DA medication as measured by LEDD, a standardized metric calculation that converts all DA medications a patient is taking into a single equivalent dose of levodopa, providing a measure of total daily DA medication burden using established methodology. A reduction in LEDD suggests that a patient requires less DA medication to manage their motor symptoms. As of the LEDD cutoff date of March 24, April 10, 2026, in the low dose cohort, two, three and four patients showed a reduction in LEDD at six, 12 and 18 months, respectively, and no patients experienced an LEDD increase. In the high dose cohort, at six months, three out of eight patients showed an LEDD reduction and one patient showed an LEDD increase; at 12 months, two out of four patients showed an LEDD reduction and one patient showed an LEDD increase; at 18 months, three out of four patients showed an LEDD reduction and one showed an LEDD increase.

Figure 1. Sustained clinically meaningful improvements observed across multiple validated PD endpoints. Data summarized above is as of February 24, April 7, 2026, except LEDD data is summarized as of March 24, April 10, 2026. A decrease (negative number) compared to baseline is an improvement for MDS-UPDRS scores and PDQ-39. The numbers in parentheses represent standard deviations. * For the four high dose patients for whom data was available at the 12-month assessment, and 18-month assessments, the baseline values for Good On Time (hrs) (hours) Hauser Diary, Off Time (hours) Hauser Diary, MDS-UPDRS part III OFF score, MDS-UPDRS part II score, and PDQ-39 were: 11.7 (0.9), 4.3 (0.9), 44.0 (4.2), 9.5 (9.3), 16.1 (15.6), respectively. For the three low dose patients in Cohort 4, no data is yet available because six months have not elapsed since dosing.

We expect to report further long-term data from the ASPIRO trial in . In addition, we plan to dose up to 12 approximately six patients with genetic PD in the ASPIRO trial. We anticipate initiating biopsy collection for the Phase 3 trial in . Following feedback from the FDA, and additional data from the ASPIRO trial, if positive, we anticipate initiating dosing patients in a Phase 3 trial in beginning with biopsy collection followed by dosing of patients in .

10 unchanged paragraphs

Stage 2 (Fibroblasts to iPSCs): The fibroblasts are converted into iPSCs through a process known as cellular reprogramming , in which a defined set of transcription factors, classically Oct3/4, Sox2, Klf4, and L-Myc, collectively referred to as the Yamanaka factors, are introduced to reset the cells gene expression and epigenetic profiles, thereby reverting them from a differentiated somatic state back to a pluripotent, embryonic-like state. We utilize Yamanaka factors licensed from third parties including iPS Academia Japan, Inc. and Sumitomo Pharma Co. Ltd. See Licensing and Collaboration Agreements below for additional information. These iPSCs are advanced to Stage 3 following characterization and QC testing for sterility, identity, purity and pluripotency (using our proprietary PluriTest).

Stage 3 (iPSCs to DANPCs) : The iPSCs derived from PD patients are first expanded to establish a stable, high-quality, iPSC population of appropriate cell number. Using our robust and proprietary differentiation iPSC platform, these cells are then efficiently and consistently differentiated into DANPCs. At the end of Stage 3, the DANPCs are harvested, filled and finished, and then cryopreserved. These DANPCs are designed to have high cell lineage fidelity and predictable functional performance, including maturity, engraftment and dopamine release. The DANPC drug product released at Stage 3 is dependent on QC testing for strength (cell concentration), purity, identity, and potency. The final product is not a homogenous cell population, and other non-DA cells are present in the final product at low percentages, including astrocyte progenitors and progenitors for cholinergic and glutamatergic neurons. Prior to patient administration, the DANPCs are shipped to the site as a sterile, cryopreserved product.

Our iPSCs are differentiated into DANPCs by recapitulating key stages of midbrain development in vitro using defined culture conditions and signaling cues. The process begins with neural induction, where iPSCs are directed away from pluripotency toward a neural fate. This is achieved through dual SMAD inhibition, which blocks BMP and TGF signaling, producing neuroectodermal cells resembling early neural progenitors. Next, these neural progenitors are patterned toward a ventral midbrain identity, the developmental origin of dopaminergic neurons. This step involves activating Sonic Hedgehog (SHH) signaling to induce ventral characteristics and WNT/ catenin signaling (via GSK3 inhibitors) to specify midbrain fate. Finally, under continued exposure to these cues and supportive growth factors combined with Notch signaling inhibition through a gamma secretase inhibitor to promote neuronal maturation, cells differentiate into dopaminergic precursors, characterized by expression of markers such as FOXA2 and OTX2. These precursor cells are designed to further mature into functional, dopamine-producing neurons upon a differentiation and after transplantation. Overall, our approach uses a stepwise, developmentally informed process designed to control signaling pathways and efficiently and reproducibly generate dopaminergic precursors from iPSCs for therapeutic application.

At the end of Stage 3, the DANPCs are harvested, filled and finished, and then cryopreserved. These DANPCs are designed to have high cell lineage fidelity and predictable functional performance, including maturity, engraftment and dopamine release. The DANPC drug product released at Stage 3 is dependent on QC testing for strength (cell concentration), purity, identity, and potency. The final product is not a homogenous cell population, and other non-DA cells are present in the final product at low percentages, including astrocyte progenitors and progenitors for cholinergic and glutamatergic neurons. Prior to patient administration, the DANPCs are shipped to the site as a sterile, cryopreserved product.

3 unchanged paragraphs

We are developing an automated, robust, modular manufacturing process for sasineprocel that we believe could reduce the manual labor required by more than 90% while still maintaining GMP requirements. Our manufacturing system incorporates two principal automated systems. The first is the Cell X platform, which can be used in Stage 1, Stage 2, and the iPSC scale-up portion of Stage 3. The Cell X platform integrates incubation within an isolation chamber, robotics, liquid handling, and optical machine vision, along with proprietary ML algorithms to evaluate fibroblast cell culture and iPSC clones for quality and to identify the most promising cells for advancement through the manufacturing process. The Cell X platform automates all standard cell culture steps for derivation of iPSCs including cell selection, reprogramming, cell removal, expansion, and harvest. We expect that each module within the Cell X platform will be capable of autonomous (self-driving) manufacturing to support manufacturing capacity for hundreds of patients on an annual basis. The second system, the Mytos device, is used in Stage 3, during which iPSC clones are differentiated into DANPCs in a closed system process. This system automates the feeding, expansion, passaging, and harvest of the iPSC into DANPCs. The Cell X platform and the Mytos devices are supplied by third party technology solution providers and are purchased and owned by Aspen. We expect the automated manufacturing process to be ready for use in early 2027, but will be required to submit an IND amendment to the FDA prior to utilizing the automated manufacturing process in our clinical trials.

2 unchanged paragraphs

Advance sasineprocel, our personalized potentially disease-modifying product candidate for PD patients, through Phase 3 trials for sporadic PD. We are continuing to advance our lead product candidate, sasineprocel, in PD, following encouraging interim results in our Phase 1/2a ASPIRO trial, including sustained improvement in PD patients motor and non-motor symptoms, and quality of life measures. We believe sasineprocel has the potential to slow or halt the progression of PD, which would transform the lives of PD patients. Following feedback from the FDA, and additional data from the ASPIRO trial, we plan to commence a Phase 3 study in patients with PD in . The initial phase of the study will involve collecting details of disease and natural history of PD and obtaining skin biopsies in in order to manufacture sasineprocel, with the goal of dosing patients in . After assessment of efficacy and safety at 18 months post dose, we plan to collect long-term safety follow-up data for a total of 15 years post dose, based on current FDA guidelines for cell and gene therapy product.

5 unchanged paragraphs

After assessment of efficacy and safety at 18 months post dose, we plan to collect long-term safety follow-up data for a total of 15 years post dose, based on current FDA requirements guidelines for cell and gene therapy product.

2 unchanged paragraphs

We are developing sasineprocel, a single-dose, autologous iPSC-based therapeutic candidate for PD that is designed to replace a patient s lost dopamine neurons. We are currently conducting the open-label Phase 1/2a ASPIRO trial of a single dose of sasineprocel in mid-stage to moderately advanced PD patients. The trial consists of four cohorts at two dose levels, both of which were anticipated to be biologically active, with sasineprocel administered as a single bilateral intracranial injection into the post-commissural putamen using well-understood, standard stereotactic neurosurgical techniques. As of the cutoff date, 14 15 patients had been dosed, with six seven participants receiving a low dose and eight participants receiving a high dose. As of the cutoff date, 12 patients had at least one six-month or later follow up evaluation. We assessed clinical outcomes every six months after administration of sasineprocel. Sasineprocel has been granted Fast Track designation from the FDA for the treatment of PD to improve motor function. A new drug or biologic is eligible for Fast Track designation if it is intended to treat a serious or life-threatening disease or condition and demonstrates the potential to address unmet medical needs for such disease or condition. However, Fast Track designation may not result in a faster development process, review, or approval compared to conventional FDA procedures, and does not increase the likelihood that sasineprocel will receive regulatory approval. In addition, because sasineprocel is designed to be administered through drug delivery devices, we anticipate that sasineprocel would be regulated as a combination product by the FDA, which requires coordination between the FDA s Center for Biologics Evaluation and Research and the FDA s Center for Devices and Radiological Health for review. For additional information, see the section titled Risk Factors Additional time may be required to obtain marketing authorizations for any of our product candidates that we develop as combination products.

8 unchanged paragraphs

Figure 4. Summary of motor and non-motor symptoms that people living with PD experience.

4 unchanged paragraphs

DBS is effective at reducing Off Time and managing tremor. It also often helps patients reduce doses of DRT, thus reducing peak-dose dyskinesia. However, it has some significant limitations. Due to the shortage of DBS-trained MDS, referrals to physicians capable of managing DBS patients can take many months. Further, only 10-15% of PD patients eligible for DBS are referred for treatment and <2% of patients elect to undergo the DBS placement procedure. Many patients are resistant to permanent placement of foreign hardware devices into their brains and elsewhere in their bodies (DBS extension wires are placed in the neck which connect the brain leads to batteries that are generally placed in the chest). Further, the hardware may limit use of diagnostic magnetic resonance imaging (MRI) scans and cause interference with electrocardiograms (ECGs) and other potentially needed emergency diagnostic studies. Additionally, it can take up to six months after an MDS recommendation to schedule DBS lead placement surgery (which is associated with a small risk of symptomatic hemorrhage), and a second surgery for battery placement is commonly performed separately. Then it can take many months working with a DBS neurologist to optimize device settings to maximize benefit and minimize stimulation-induced side effects. Moreover, the batteries for the system need to be periodically replaced. The DBS hardware may fail or become infected, often necessitating additional surgeries or removal of the hardware and sometimes long courses of antibiotics. DBS has not been shown to slow disease progression be in mid-stage to moderately advanced PD patients and can potentially worsen cognition, gait, speech and other axial symptoms.

2 unchanged paragraphs

There is an urgent need to develop disease-modifying therapies that sustain dopamine production and have an impact on both motor and non-motor symptoms, but current approved therapies are focused on improving motor symptoms. Longer acting forms of DRT will likely have the same challenges for chronic PD patients as current L-dopa therapy. Maintenance or replacement of DA neurons and supporting cell types may represent a more promising approach for a true disease-modifying treatment with long-term effectiveness. Cell replacement therapy represents a promising option for a therapy that can provide long-term benefit from a single administration. Of the estimated more than one million people in the United States affected by PD, we believe that approximately 300,000 of such patients are refractory to DRT and that approximately half of those patients would be eligible for a cell replacement therapy surgery. Previous studies have demonstrated that transplantation of human fetal, ventral-mesencephalic tissue containing DA neurons can lead to long-lasting (greater than 10 years) engraftment of DA neurons and improvements in the motor symptoms of PD. These findings provide historical support for the concept of DA cell replacement and therapeutic strategy. Current cell replacement strategies under investigation for PD include transplantation of allogeneic and autologous stem cell-derived DA neuron precursors.

6 unchanged paragraphs

A third-party preclinical study conducted by the University of Wisconsin-Madison (Tao et al., Nature Medicine, 2021) comparing autologous to allogeneic iPSC-derived DA neuronal cell transplantation in NHP models of PD over a two-year period, without immunosupression, immunosuppression, was conducted to evaluate motor function, graft survival and integration, among other things. This study demonstrated improvements in motor behavior following transplantation of DA progenitor cells, with autologous grafts associated with approximately 40% to 60% improvement in motor function, sustained over a 24-month post-transplant period, compared with allogeneic grafts in the absence of immunosuppression (Figure 5 4 below). In addition, histological analyses showed that autologous grafts differentiated into tyrosine hydroxylase (TH)-positive DA neurons and exhibited extensive neurite and axonal outgrowth extending from graft sites into surrounding host tissue, consistent with reconstruction of DA neural circuitry. In contrast, allogeneic grafts in the same model demonstrated more limited neurite outgrowth and reduced integration in the absence of immunosuppression. These findings suggest that autologous DA progenitor transplantation may support more robust neural integration and restoration of DA signaling compared with donor-derived cells when immunosuppression is not administered. However, allogeneic cell therapies in clinical settings are generally administered with immunosuppression, and the results of this study may not be predictive of patient outcomes under conditions in which immunosuppression is used. To our knowledge, there are no published preclinical studies directly comparing autologous to allogeneic dopaminergic precursor cell transplantation under immunosuppression in comparable non-human primate models of Parkinson s disease.

Figure 5. 4. Monthly clinical rating score (CRS) of the monkeys receiving allogeneic or autologous transplantation from 12 months before transplantation to 24 months after transplantation. The transplantation occurred at month 0. Lines show mean values for every 3 months from the allogeneic group or the autologous group. Significance was assessed by Friedman test (non-parametric statistical test) (d, e); * p < 0.05, ** p < 0.01.

2 unchanged paragraphs

Personalized approach: Sasineprocel is an autologous product candidate designed to minimize the risk of immune rejection and eliminate the need for long-term immunosuppression and its associated risks. In addition, based on market research, we believe patients prefer the personalized approach of autologous cell therapy as compared to gene or allogenic therapies.

Proprietary cell composition: Sasineprocel s proprietary composition of DANPCs, together with supportive CNS and glial progenitors and other neuronal cells, is designed to create a biologically active microenvironment that may support restoration of neural circuitry and synapse formation. We believe this differentiated cellular composition may contribute to the motor meaningful and non-motor sustained improvements observed in PD patients in the ASPIRO trial.

Precise and streamlined delivery: Sasineprocel is administered through a minimally invasive procedure using well-understood standard of care stereotactic neurosurgical techniques, which key opinion leaders reported being amenable to. The product is thawed at the time of surgery for immediate administration and does not require on-site cell processing or testing capabilities. Following administration, sasineprocel requires no device maintenance, programming, or ongoing optimization, differentiating it from device-based therapies such as DBS.

2 unchanged paragraphs

We are currently conducting the open-label Phase 1/2a ASPIRO trial of a single dose of sasineprocel in patients with PD. Promising interim clinical data from both the high and low dose cohorts suggests that the administration of sasineprocel could potentially lead to significant long-term clinical benefit for PD patients across both motor and non-motor symptoms and potentially slow or halt the progression of the disease. We expect to report 24-month data from four patients in the low dose cohort and 18-month data from four patients in the high dose cohort in . In addition, we plan to dose up to 12 approximately six patients with genetic PD in the ASPIRO trial. We anticipate initiating biopsy collection for the Phase 3 trial in . Following feedback from the FDA, and additional data from the ASPIRO trial, if positive, we anticipate initiating dosing patients in a Phase 3 trial in .

3 unchanged paragraphs

We are conducting a first-in-human, multi-center, open-label Phase 1/2a ASPIRO trial evaluating the safety, tolerability, and efficacy of the intracranial injection of sasineprocel in patients with mid-stage to moderately advanced PD. The study s primary objective is to assess the safety and tolerability of bilateral administration of sasineprocel into the post-commissural putamen. The study s secondary and other exploratory objectives are to evaluate the potential efficacy of sasineprocel, measured by changes from baseline in multiple patient- and clinician-reported PD-specific outcomes. These include changes in MDS-UPDRS Parts I-IV, Hauser diary (to measure Good On time, defined as time without troublesome dyskinesia), NMSS, and quality of life measures including PDQ-39. These secondary endpoints are validated endpoints used in previous PD registrational clinical trials for drugs such as RYTARY approved in 2015 and VYALEV (foscarbidopa/foslevodopa) approved in 2024.

2 unchanged paragraphs

We use a streamlined, precise and minimally invasive process for sasineprocel administration that generally allows patients to be discharged the next day. Prior to administration, the drug product arrives as cryopreserved cells in a vial, which is warmed at bedside one hour before surgery. The product is delivered using well-understood, standard stereotactic neurosurgical techniques. The administration is performed through a single 4mm burr hole with bilateral cell deposition into the putamen over a duration of approximately 90 minutes.

1 unchanged paragraph

Beyond these changes being clinically meaningful from baseline, third-party natural history studies suggest patients with PD worsen across all these measures. For instance, third-party natural history studies suggest that MDS-UPDRS Part III OFF and MDS-UPDRS Part II scores should worsen by approximately 2.4 points and one point per year, respectively, on standard of care.

Quality of Life and Non-Motor Symptoms Assessments

Non-motor symptoms are being assessed using the NMSS, a 30-item, clinician-rated scale specifically designed to measure non-motor symptoms in people with PD. NMSS is a well-understood and validated measure of non-motor symptoms for PD. The scale evaluates the severity and frequency of non-motor symptoms across nine domains, including cardiovascular issues and falls, sleep/fatigue, mood/cognition, perception/hallucinations, attention/memory, gastrointestinal, urinary, sexual function, and miscellaneous (including pain, smell, weight change, and sweating). These non-motor symptoms often have as much of an impact on quality of life as the motor symptoms most people associate with PD, and the NMSS has demonstrated correlation with quality of life, disease severity, and motor function measures of PD. Each item is scored on a scale of 0-12 (taking severity and frequency into account), and the total score is the sum of the 30 items across all nine domains, with higher scores indicating worse symptoms. In several participants, treatment with sasineprocel resulted in demonstrated improvements in several non-motor symptoms and quality of life domains. Based on available data as of February 13, 2026, treatment with sasineprocel resulted in improvement in several domains of NMSS, as shown in Figure 9 below.

Figure 9. Data summarized above is as of February 13, 2026. Each item is rated for severity (0 to 3) and for frequency (1 to 4). The numbers in parentheses represent standard deviations. Item score is severity multiplied by frequency. Domain score is sum of items. Bold indicates improvement compared to baseline.

During the course of the ASPIRO trial, we experienced a delay in patient dosing due to issues with the design of the syringe used as part of our drug delivery system. The FDA imposed a clinical hold on the syringe used as part of our drug delivery system between January 2023 and August 2023. We worked with the supplier to design and validate a new syringe configuration, which has been implemented for subsequent dosing. We do not currently have arrangements in place for redundant supply or a second source for all required materials and components, including the delivery device, used in our clinical trials. See Risk Factors Risks Related to Our Reliance on Third Parties for additional information.

Figure 6. 5. Schematic representation of Aspen s Phase 1/2a ASPIRO trial with endpoints.

As of April 7, 2026, the data cutoff date, sasineprocel was generally well tolerated with only mild to moderate adverse events a majority of reported with no adverse events related being mild to sasineprocel. In moderate. As of the cutoff date, 15 patients enrolled, of which 14 have had been dosed, there were 55 treatment emergent with seven participants receiving a low dose and eight participants receiving a high dose. Among the patients dosed, 58 treatment-emergent adverse events (TEAEs) one were reported. There was no evidence of which, graft-induced dyskinesias or graft rejection, and no clinically significant hemorrhages were observed post-operatively. As sasineprocel is autologous, with no requirement for immunosuppression, there were no immunosuppression-related events. Only one TEAE, myoclonus (sudden, uncontrollable muscle movement), was deemed to be considered possibly related to sasineprocel, There was no graft induced dyskinesia reported. One participant had mild asymptomatic hemorrhage during the surgical procedure that resolved immediately. with sertraline, a selective serotonin reuptake inhibitor, identified as a co-suspect medication. One participant had two serious adverse events related to the surgical procedure (swollen tongue (neck swelling and dysphagia due to intubation in the prone position and stroke due to pre-operative interruption of anticoagulants that the patient was taking for a history of deep venous thrombosis). These events have resolved. The most commonly reported TEAEs, defined as occurring in 10% or more of patients, were related to the surgery, including incision site pain, swollen tongue, headache, infusion site pain, glossodynia, hypoesthesia, and oropharyngeal pain. As of the data cutoff date, there were no study discontinuations and no symptomatic 12 patients had at least one six-month or later follow up evaluation. Two patients had intracranial hemorrhages not requiring any surgical treatment. Of these two patients, one patient had no associated symptoms and the other, who had a history of migraine, had a headache that resolved, with levetiracetam identified as a co-suspect medication.

We are assessing clinical outcomes every six months after administration of sasineprocel. As of the cutoff date, we observed improvements across several secondary and exploratory endpoints, including changes in Good On Time (On time without troublesome dyskinesia normalized to 16 hours of awake time), MDS-UPDRS Part III OFF. Consistent with these motor improvements, we also observed improvements in activities of daily living and quality of life measures assessed by MDS-UPDRS Part II ON and PDQ-39 scores, as summarized below. Certain of the secondary endpoints used in this trial, including Good On Time and MDS-UPDRS Part III OFF, are validated registrational endpoints used in previous PD registrational clinical trials. Each of these outcomes The mean improvements at 12 18 months for Good On Time and MDS-UPDRS Part III OFF scores in both cohorts as well as 18 months for the low dose cohort, were above clinically meaningful change benchmarks. which we estimated based The mean PDQ-39 and MDS-UPDRS Part II ON published literature. scores improved above clinically meaningful change benchmarks in the low dose cohort and were stable in the high dose cohort at 18 months. FDOPA PET imaging is also being used to evaluate the engraftment of cells. FDOPA PET imaging showed elevated FDOPA uptake values at 6, 12, and 18 months following sasineprocel administration compared to baseline, which is evidence of the survival, viability, and integration of transplanted iPSCs. Clinically meaningful change benchmarks are reviewed on an ongoing basis during the trial and reflect management s belief based on a review of published literature, regulatory agency guidelines and precedent in PD clinical research, and discussions with key opinion leaders in the field. The benchmarks have not been discussed with the FDA or any other government regulatory authority, and have not been independently validated by any third parties.

Additionally, the ASPIRO trial is exploring changes in DA medication as measured by LEDD, a standardized metric that converts all DA medications a patient is taking into a single equivalent dose of levodopa, providing a measure of total daily DA medication burden. A reduction in LEDD suggests that a patient requires less DA medication to manage their motor symptoms. As of the LEDD cutoff date of March 24, April 10, 2026, in the low dose cohort, two, three and four patients showed a reduction in LEDD at six, 12 and 18 months, respectively, and no patients experienced an LEDD increase. In the high dose cohort, at six months, three out of eight patients showed an LEDD reduction and one patient showed an LEDD increase; at 12 months, two out of four patients showed an LEDD reduction and one patient showed an LEDD increase; at 18 months, three out of four patients showed an LEDD reduction and one showed an LEDD increase.

Figure 7. 6. Sustained clinically meaningful improvements observed across multiple validated PD endpoints. Data summarized above is as of February 24, April 7, 2026, except LEDD data is summarized as of March 24, April 10, 2026. A decrease (negative number) compared to baseline is an improvement for MDS-UPDRS scores and PDQ-39. The numbers in parentheses represent standard deviations. * For the four high dose patients for whom data was available at the 12-month assessment, and 18-month assessments, the baseline values for Good On Time (hrs) (hours) Hauser Diary, Off Time (hours) Hauser Diary, MDS-UPDRS part III OFF score, MDS-UPDRS part II score, and PDQ-39 were: 11.7 (0.9), 4.3 (0.9), 44.0 (4.2), 9.5 (9.3), 16.1 (15.6), respectively. For the three low dose patients in Cohort 4, no data is yet available because six months have not elapsed since dosing.

Beyond these changes being what we believe to be clinically meaningful from baseline, third-party natural history studies suggest patients with PD worsen across all these measures. Parkinson s Progression Markers Initiative, or PPMI, is a large, internationally used research data set designed to collect standardized clinical data over time to better understand how PD starts and progresses. These PPMI data suggest progressive worsening of approximately two points per year on the MDS-UPDRS Part III OFF scale. In contrast, sasineprocel, including eight patients (low dose; n=4, high dose; n=4), shows a mean decrease, or improvement, at six, 12, and 18 months of 14.6, 14.5, and 16.1 points, respectively. Figure 7 below p resents the mean change from baseline in MDS-UPDRS Part III OFF scores for each patient at the six-month, 12-month, and 18-month assessments together with the mean change from baseline observed in natural history study patients, reflecting the progressive worsening expected in PD patients over time .

Figure 8 below presents the Good On Time for each patient at each available assessment, as measured using the Hauser diary, together with the mean Good On Time hours for the low dose and high dose cohorts at each assessment, in each case as of the February 24, April 7, 2026 efficacy data cutoff. The mean Good On Time hours for each cohort at each assessment, as shown in Figure 8 below, reflect the average of the individual patient Good On Time hours at such assessment. As measured by mean change from baseline per patient, the low dose cohort showed a mean increase of 2.2 hours at 18 months, and the high dose cohort showed a mean increases increase of 2.3 hours at 6 months and 2.4 2.7 hours at 12 18 months. For the low dose cohort, there were four patients in each of the assessments shown. For the high dose cohort, there were eight patients for the baseline Day 90 and Day 180 assessments. shown and four patients for the Day 270 and Day 365, and 18-month assessments shown; had four patients; the mean baseline and standard deviation for the four patients shown at Day 270 and Day 365, and 18 months was 11.7 (0.9).

Quality of Life Assessments

In addition to preliminary safety and motor function data, we observed improvements in quality of life and non-motor symptoms following the administration of sasineprocel.

Quality of life improvements are being assessed using PDQ-39, a 39-item, patient reported questionnaire used to measure health related quality of life in people with PD. PDQ-39 is the most widely used disease specific quality of life measure for PD. The questionnaire asks patients how often, over the past month, they have experienced difficulties related to PD across eight domains, including mobility, activities in daily living, emotional well-being, stigma associated with disease, social support, cognition, communication, and bodily discomfort. Each domain is scored on a standard scale ranging from 0 100 and the total score is the mean of the eight subdomains, with higher values indicating greater disease burden. As of the cutoff date, patients in Cohort 1 (low dose; n=4) and Cohort 2 (high dose; n=4), treatment with sasineprocel resulted in a reduction in total PDQ-39 score at 12 18 months of 7.6 5.0 and 6.1, 3.8, respectively, demonstrating meaningful improvements in quality of life. As of April 7, 2026, the data cutoff date, the total PDQ-39 score at 18 months improved (decreased) in three out of eight patients, with a mean 21% reduction from baseline, remained stable in four patients, and worsened in one patient.

1 unchanged paragraph

We have further incorporated DHT using the Strive PD app from Rune technologies and a home-based monitoring device from Emerald Innovations to evaluate mobility and sleep by continuous monitoring. We observed improvements in REM sleep latency, as measured using Emerald Innovations technology, in five out of six patients at 12 months; we believe this improvement was associated with quality of life improvements in PDQ-39. As measured by NMSS, patients sleep/fatigue measurements improved from baseline at each time point measured in the low dose and high dose cohorts.

We have explored endpoints across the Scales for Outcomes in Parkinson s Disease Autonomic (SCOPA-AUT) measurements, a validated, patient reported questionnaire specifically designed to assess autonomic nervous system symptoms in people with Parkinson s disease, and the Montreal Cognitive Assessment (MoCA) measurements, the most widely used brief cognitive screening tool for detecting mild cognitive impairment (PD MCI) and Parkinson s disease dementia (PDD). At 18 months, out of eight patients (low dose; n=4, high dose; n=4), we saw improvements in SCOPA-AUT in three patients, stability in four patients, and worsening in one patient. At 18 months, out of eight patients (low dose; n=4, high dose; n=4), we observed stability in MoCA in all eight patients.

The Gait Axial subscore, a clinical metric derived from MDS-UPDRS Part III, improved in 7 of 8 patients at 12 18 months, with a mean 46% increase, as shown in Figure 10 9 below. Low gait axial subscores are associated with reduced fall risk. DRT typically has little effect on the axial symptoms of PD, suggesting the consistent improvement is potentially the result of neural circuitry reconstruction following the administration of sasineprocel. Mobility (gait, step count, stair ascent and descent speed, and sleep) was improved in a majority of patients measured by both forms of DHT.

We evaluated FDOPA PET imaging to assess DA activity in the putamen following administration of sasineprocel. FDOPA PET is a specialized neuroimaging technique that uses a radiolabeled dopamine precursor to assess DA activity in the striatum, including the putamen, a brain region significantly affected in PD. FDOPA PET showed increased FDOPA uptake at six, 12 and 18 months following sasineprocel administration compared to baseline. These data support continued clinical evaluation of sasineprocel as a cell replacement therapy for PD.

3 unchanged paragraphs

Our preclinical studies have demonstrated successful engraftment and maturation following intracerebral transplantation of DANPCs and subsequent recovery of DA signaling deficits in a rodent 6-OHDA model of PD. Transplantation of DANPCs from four different PD donors into the denervated striatum resulted in behavioral recovery (decrease in amphetamine-induced rotations) over a 28-week rodent study (Figure 11A 10A below). Histological analyses showed survival of transplanted cells within the target region and differentiation into TH-positive DA neurons. These cells exhibited robust neurite and axonal outgrowth extending into the surrounding host tissue, consistent with integration into existing neural circuitry (Figure 11B 10B below).

Figure 11. 10. (A) Mean net amphetamine-induced rotations per minute, from Baseline (pre-dosing) until 28-weeks post-dosing. (B) Representative histological images of a series sections from a rodent brain stained for TH (i), magnified image of the striatum stained for TH (ii), human cytoplasm indicating presence of human cells (iii), human nuclei indicating presence of human cells (iv), increased magnification of the grafted cells stained for TH (v) and human cytoplasm (v).

6 unchanged paragraphs

Figure 12: 11. A) Immunocytochemistry for DAN markers FOXA2 and TH at Day 40 post differentiation. Scale bar=100 m. The four different lines show similar morphologies of TH+ neurons and a similar abundance of FOXA2+ cells. B) Quantification of FOXA2+ and TH+ cells normalized to total DAPI+ cells at Day 40 (n=3 lines/group).

4 unchanged paragraphs

The planned Phase 3 trial is intended to evaluate the safety and efficacy of sasineprocel in a larger patient population and to support a potential Biologics License Application (BLA). In contrast to The Phase 1/2a ASPIRO trial, the Phase 3 trial is expected to include a control group, prespecified primary and secondary efficacy endpoints, exploratory endpoints and longer-term assessments designed to evaluate durability of clinical effects.

Aspen intends to leverage insights from the Phase 1/2a ASPIRO trial including dose selection, delivery procedures, endpoint performance, and manufacturing experience to inform the design of the Phase 3 trial. We plan to engage with regulatory authorities to obtain feedback on key aspects of the Phase 3 program, including patient population, endpoint selection, statistical considerations, and trial design features.

7 unchanged paragraphs

In September 2024, we entered into a Main Services Agreement and related order forms and schedules (the Mytos Agreement ) with Mytos Bio Limited ( Mytos ). Under the Mytos Agreement, Mytos supplies us with automated cell culture devices, along with related software licensing and associated services. We use the Mytos iDEM Triple device and the iDEM platform in Stage 3 of our manufacturing process for sasineprocel to automate key cell culture steps during the differentiation process. Mytos provides cloud-based software to operate the device, installation services, and additional development services to validate the device for compatibility with our manufacturing requirements.

Under our order form with Mytos, we may purchase Mytos iDEM Triple devices at a purchase price in the low hundreds of thousands of dollars, per device. The Mytos Agreement also contemplates various installation fees in a range of tens of thousands of dollars, depending on the number of devices. The Mytos Agreement further provides us with a license to the basic tier software required to operate the device, which is provided at no additional charge for so long as we own the device.

We retain all right, title, and interest in and to all data, protocols, and outputs arising from our use of the Mytos iDEM Triple device and related software. Mytos retains all intellectual property rights in the device, software, and services, including any improvements arising from our use thereof. We have granted Mytos a limited license to use our data and outputs for the purpose of providing the goods, software, and services to us in accordance with the Mytos Agreement and for developing improvements to the Mytos iDEM Triple device and/or software during the term of the agreement.

The Mytos Agreement has an initial term of two years from the effective date and automatically renews for successive one-year periods unless terminated. We may terminate the agreement for convenience upon 30 days prior written notice, subject to payment of any authorized costs and expenses incurred and de-installation fees. Either party may also terminate the agreement for (i) material breach (subject to a 30-day cure period for remediable breaches), (ii) non-payment that remains outstanding more than 30 days after written notice, or (iii) if the other party suspends or ceases its business or suffers an insolvency event. In addition, Mytos may terminate the agreement immediately if there is a change of control of the Company that results in us being held by a direct competitor of Mytos as defined in the Mytos Agreement.

We are responsible for all risk and liability arising from reliance on the outputs of the device. We may not sell the device to any third party without Mytos prior written consent. We paid Mytos $1.5 million and $0.2 million during the years ended December 31, 2025 and 2024.

We rely on third parties for certain materials and components for sasineprocel and other product candidates.

In November 2021, we entered into a services agreement (hereinafter, the Veranex Agreement ) with Ximedica, LLC ( Ximedica ), which was acquired by Veranex, Inc. ( Veranex ) in June 2021. The Veranex Agreement was assigned from Ximedica to Veranex on or about October 18, 2023. Under the Veranex Agreement, Veranex provides development and manufacturing services for metered delivery syringes used as part of our drug delivery system in connection with our clinical programs. Veranex performs services for us on a project basis. Upon acceptance of the proposal made in connection with the Veranex Agreement, a non-material payment was made as a deposit for the estimated first month s service and expenses. Following the initial deposit, Veranex is to issue monthly invoices for work in progress. Each invoice will include amounts for billable time, plus out-of-pocket and other expenses incurred during the monthly period preceding the invoice. All such out-of-pocket and project-related expenses (other than billable time) are invoiced at cost, plus a percentage markup in the high teens to cover administration and handling.

The Veranex Agreement does not have a fixed term or expiration date. However, we may cancel any project under the Veranex Agreement, at any time, with or without cause, upon 90 days prior written notice, subject to our obligation to pay for all work delivered and billable work performed during the notice period, as well as expenses and service costs incurred through the date of cancellation.

The Veranex Agreement provides that all project-related work product developed by Veranex will be delivered to us and become our sole property upon payment of any invoices due in full, and Veranex has assigned to us all right, title, and interest therein. Notwithstanding the foregoing, Veranex retains ownership of certain minor pre-existing code, programming and/or components, works and elements (such as tooling code, scripts, tools, subroutines, algorithms and plug-ins) and related know-how incorporated in the project work product, as well as enhancements and modifications to the foregoing, that were not specifically developed for our projects. Veranex has granted us a royalty-free, fully-paid-up, irrevocable, transferable, sublicensable, worldwide, perpetual license to use, reproduce, modify, publicly distribute and perform, display and otherwise commercially exploit such Veranex intellectual property in connection with our use and exploitation of the project work product under the Veranex Agreement.

We and Veranex are subject to mutual confidentiality obligations with respect to proprietary information disclosed pursuant to the Veranex Agreement, which obligations survive any project termination.

We are responsible for testing the project work, for assessing whether the project work infringes the intellectual property rights of any third parties, and for securing any patent protection. We paid Veranex $1.0 million and $0.5 million during the years ended December 31, 2025 and 2024.

In January 2022, we entered into a Master Supply Agreement (the ClearPoint MSA ) with ClearPoint Neuro, Inc. ( ClearPoint ). Under the ClearPoint MSA, ClearPoint manufactures and supplies us with specialized neurosurgical products, including its SmartFlow ventricular cannulas. We use the ClearPoint SmartFlow cannula as part of our drug delivery system for the administration of sasineprocel.

The ClearPoint MSA sets forth the purchase price for the products. ClearPoint invoices us in accordance with the invoice schedule set forth in the applicable purchase order or SOW. The initial term of the ClearPoint MSA ends in January 2027 and will automatically renew for successive one-year periods unless either party provides at least 180 days written notice of its intent not to renew prior to the expiration of the then-current term. In addition, either party may terminate the ClearPoint MSA for material breach of the agreement, subject to a 30-day cure period. The ClearPoint MSA does not provide either party with a right to terminate for convenience during the term. If the ClearPoint MSA is terminated for any reason other than ClearPoint s material breach, we are responsible for any non-cancelable costs or expenses incurred by ClearPoint in connection with third-party obligations under outstanding purchase orders or statements of work.

We are solely responsible for obtaining all regulatory approvals relating to our therapies incorporating ClearPoint products, including the ClearPoint SmartFlow cannula. ClearPoint retains all right, title, and interest in and to the products sold to us pursuant to the ClearPoint MSA and all intellectual property rights related thereto, including sole ownership of any improvements, additions, or variations to the products, whether or not made at our request, except to the extent otherwise set forth in a development agreement with respect to custom products that have been enhanced, improved, or customized by ClearPoint solely for our use. ClearPoint further has the right to sell, offer, license, or otherwise commercialize the products and services covered by the ClearPoint MSA to third-party customers. We paid ClearPoint $0.3 million during each of the years ended December 31, 2025 and 2024.

1 unchanged paragraph

As described above, our production process is performed in three stages. Stage 1 (skin to fibroblast) has a manufacturing duration of approximately three weeks. Stage 2 (fibroblasts to iPSCs) has a duration of approximately eight weeks. Stage 3 (iPSCs to DANPCs) has a duration of approximately five weeks. Following each stage, we complete QC testing which typically takes a total of four to five weeks. Intermediate products (that is, products following Stage 1 and Stage 2) can be conditionally released during QC testing in approximately one to two weeks, which could speed up the overall manufacturing process.

3 unchanged paragraphs

The overall manufacturing process for the dose prep formulation and the thaw-and-inject formulation are the same with the exception of the post harvest downstream volume reduction step, the formulation step, the excipients utilized, the fill step, and the final product container. For dose prep formulation, the final cell concentration is 6.7 x 106 cells/mL filled at 1.5 mL in a 2mL cryovial whereas for the thaw-and-inject formulation, the final cell concentration is 1.0 x 108 cells/mL filled at 0.5mL in a 2mL CellSeal vial.

The thaw and inject formulation of sasineprocel (ANPD001 Suspension) was evaluated in a series of nonclinical studies designed to assess location, engraftment, and safety following direct intracerebral administration. In rodents, a non GLP engraftment study and a pivotal single dose GLP toxicity study demonstrated that ANPD001 Suspension was well tolerated and resulted in persistent engraftment of human cells with comparable average graft size and number of mature dopaminergic neurons after 3-month in life maturation in a side-by-side evaluation with dose prep formulation (ANPD001 Injectable Suspension) and human cells remained localized to the target striatal region, with no evidence of migration outside the brain. No adverse effects on clinical observations, body weights, functional assessments, clinical pathology, or macroscopic or microscopic pathology were observed. These studies support the safety of the thaw and inject formulation and its suitability for clinical administration without additional dose preparation steps.

2 unchanged paragraphs

Automation is intended to reduce manual handling, improve process safety and consistency, and enable parallel processing of multiple patient-specific manufacturing runs within a controlled footprint. We also automatically capture use automated data capture and analytical tools to support in-process monitoring, quality assessments, and manufacturing decision-making.

1 unchanged paragraph

Figure 13. 12. A summary of our plans for autonomous, automated cell manufacturing to support potential future demand.

2 unchanged paragraphs

Key competitive factors affecting thel the success of our product candidates, if approved, are likely to be efficacy, safety, convenience, presentation, price and the availability of reimbursement from government and third-party payors. Our competitors may obtain FDA or other regulatory approval for their products more rapidly than we may obtain approval for ours, which could result in our competitors establishing a strong market position before we are able to enter the market. We anticipate that we will continue to face increasing competition as new therapies, technologies and data emerge within the field of neurodegenerative disease and, more specifically, for the treatment of PD.

5 unchanged paragraphs

As of March 2026, our patent portfolio included 3 granted U.S. patents, approximately 15 granted international patents, and approximately 63 pending patent applications across 16 patent families, including the nine families identified in more detail below. Our granted international patents are held in the following jurisdictions: the United Arab Emirates, Australia, the European Patent Convention (validated in Switzerland, Spain, Great Britain, Ireland, Turkey, and the Unitary Patent territory), Hong Kong, Israel, Japan, Mexico, and Saudi Arabia. We also have pending patent applications in numerous international jurisdictions, including the United Arab Emirates, Australia, the European Patent Convention, Hong Kong, Israel, Japan, Mexico, Saudi Arabia, Brazil, Canada, China, India, Singapore, South Korea, and before the World Intellectual Property Organization (WIPO) under the Patent Cooperation Treaty. Our patent applications, if granted, are designed to provide protection for sasineprocel and our platform technologies, including:

3 unchanged paragraphs

These patent families include granted patents in the United States and other foreign jurisdictions. See Intellectual Property for more information. These patent families also include pending Patent Cooperation Treaty (PCT) applications, pending United States patent applications, and pending patent applications in other foreign jurisdictions. These patents, and if issued these patent applications, will expire from 2041-2046, without taking into account any possible patent term adjustment or extension and assuming payment of all applicable maintenance, renewal, annuity or other governmental fees.

23 unchanged paragraphs

We seek trademark protection in the United States and in certain other jurisdictions where available and when we deem appropriate. We currently have registrations for our Aspen Neuroscience and the leaf logo. For additional information on the risks associated with our trademark strategy and portfolio, please see the section titled Risk Factors Risks Related to Our Intellectual Property.

1 unchanged paragraph

Our patent portfolio includes both internally developed intellectual property and technology licensed from third parties. We have obtained licenses to key foundational technologies important to supporting the manufacturing process for sasineprocel, including:

iPS Academia Japan, Inc.: Methods for reprogramming differentiated cells into iPSCs using the Yamanaka factors. The licensed patents include six patent families covering iPSC cell reprogramming technologies, with issued patents and pending applications in the United States, Japan, and numerous other jurisdictions worldwide, including Australia, Canada, China, Europe, India, Israel, Korea, Mexico, Singapore, and others. This license is non-exclusive, non-transferable, and requires payment of an upfront fee, annual maintenance fees, milestone payments upon achievement of specified regulatory and commercial milestones, and royalties in the low single digits on net sales of licensed products.

Sumitomo Pharma Co. Ltd: Use of Sendai viral vectors encoding the Yamanaka factors for reprogramming differentiated cells into iPSCs. The licensed patents include five issued U.S. patents directed to methods of producing induced pluripotent stem cells using Sendai virus vectors, together with corresponding foreign patents and applications. This license is a non-exclusive sublicense of rights originally granted by ID Pharma Co., Ltd. to Sumitomo, and requires payment of annual license fees, milestone payments upon achievement of specified sales thresholds, and royalties in the low single digits on net sales of licensed products.

The Scripps Research Institute (TSRI): Methods for differentiating DA neurons from iPSCs and bioinformatics assays for characterizing neuronal cell types. There are no patents currently associated with this license. This license requires payment of royalties in the low single digits on net sales of licensed products.

Cell X Technologies, Inc. (sublicensed from the Cleveland Clinic Foundation): Systems and methods for automated manufacturing detection, analysis, isolation, and harvesting of DANPCs. biological objects, including iPSCs, as well as related image analysis technologies. The licensed patents include four issued U.S. patents and a pending European patent application directed to automated cell culture systems and machine vision-based cell selection. This sublicense is exclusive within the licensed field and territory. This license requires milestone payments upon achievement of specified development and regulatory milestones but does not require royalty payments. We are currently in discussions regarding the terms of this license in connection with our long-term automation strategy. If we are unable to maintain access to the licensed technology on commercially reasonable terms, we may need to develop alternatives or rely on less automated processes, which could increase costs and/or limit scalability.

1 unchanged paragraph

66 unchanged paragraphs

4 unchanged paragraphs

2 unchanged paragraphs

1 unchanged paragraph

and 4 more changes in the filing

Management 4 changes

28 unchanged paragraphs

Thomas Daniel, M.D . Dr. Daniel has served on our board of directors since March 2020. Recently, he served as a Venture Partner at ARCH Venture Partners, a venture capital firm, from October 2016 through June 2021. Dr. Daniel currently serves as Chairman of Gate Bioscience, which he joined in June 2022. Dr. Daniel was previously at Celgene Corporation, a pharmaceutical company, where he served as Chairman of Research from January 2016 until June 2016, President of Research and Early Development from December 2006 to January 2016, and Executive Vice President and President of Research and Early Development from February 2012 until January 2016. Prior to joining Celgene Corporation, Dr. Daniel served as the Chief Scientific Officer and director at Ambrx, Inc., a biopharmaceutical company. Prior to Ambrx, Inc., Dr. Daniel served as Vice President of Research at Amgen Inc., a biopharmaceutical company, where he was research site head of Amgen Washington and therapeutic area head of inflammation. Dr. Daniel also served as the Senior Vice President of Discovery Research at Immunex Corporation, a biopharmaceutical company, until its acquisition by Amgen. Since 2017, Dr. Daniel has served as a director at Vividion Therapeutics, a biopharmaceutical company that was previously publicly-held. Dr. Daniel has also served on the board of Gossamer Bio, a biopharmaceutical company, since January 2018. Dr. Daniel serves as a member of the Biomedical Science Advisory Board of Vanderbilt University Medical Center and chairs the Board of Overseers for The Scripps Research Institute. He also serves as senior advisor to several private biotechnology companies. Previously, Dr. Daniel served as a member of the board of directors of VIR Biotechnology, a biotechnology company, from January 2017 to August 2019 and Larimar Therapeutics, a biotechnology company, from March 2016 to May 2022. A nephrologist and former academic investigator, he was previously C.M. Hakim Professor of Medicine and Cell Biology at Vanderbilt University. Dr. Daniel received his M.D. from the University of Texas, Southwestern, trained in molecular genetics at UTSW, and completed his residency in Internal Medicine at Massachusetts General Hospital.

1 unchanged paragraph

from The Wharton School of the University of Pennsylvania, where he graduated with honors as a Siebel Scholar and Palmer Scholar.

Douglas Fisher, M.D . Dr. Fisher has served on our board of directors since March 2022. Dr. Fisher is currently a Partner at Revelation Partners, LLC, a venture capital firm, where he has worked since March 2020. Prior to joining Revelation, Dr. Fisher was a Partner and Executive-In-Residence at InterWest Partners LLC (InterWest), a private equity firm, where he focused on biopharma, diagnostics, and medical device investing. While at InterWest, Dr. Fisher also served as the Chief Business Officer of Sera Prognostics, Inc., a diagnostics company. Dr. Fisher previously served on the board of Precipio, Inc., a biotechnology company, from September 2017 through January 2024 and Obalon Therapeutics, Inc., a medical technology company, from May 2012 through June 2021. Dr. Fisher received an A.B. in economics with honors and distinction, and a B.S. in biology with distinction, from Stanford, where he graduated Phi Beta Kappa. He holds an M.D. from the University of Pennsylvania School of Medicine and an M.B.A. from The Wharton School of the University of Pennsylvania, where he graduated with honors as a Siebel Scholar and Palmer Scholar.

7 unchanged paragraphs

Peter A. Thompson, M.D . Dr. Thompson has served as a member of our board of directors since March 2020. Dr. Thompson is a Member Partner at OrbiMed Advisors LLC, an investment firm, where he has served in various roles of increasing responsibility since 2010. Dr. Thompson currently serves on the boards of directors of ARS Pharmaceuticals, Inc. (formerly Silverback Therapeutics, Inc.), a biopharmaceutical company, Corvus Pharmaceuticals, Inc., a biopharmaceutical company, Edgewise Therapeutics, Inc., a biopharmaceutical company and Sionna Therapeutics, Inc., a biopharmaceutical company, as well as several private companies. Previously, Dr. Thompson served on the boards of Alpine Immune Sciences, Inc., a biotechnology company, Decibel Therapeutics, Inc., a biotechnology company, Janux Therapeutics, Inc., a biopharmaceutical company, and PMV Pharmaceuticals, Inc., a precision oncology company. Dr. Thompson also previously served in executive leadership roles at Trubion Pharmaceuticals, Inc., Chiron Corporation, and Becton, Dickinson and Company. Dr. Thompson is an Affiliate Professor of Neurosurgery at the University of Washington. In addition, Dr. Thompson holds numerous patents and is a board-certified internist and oncologist. Dr. Thompson holds a Sc. B. in Molecular Biology and Mathematics from Brown University and an M.D. from Brown University Medical School.

52 unchanged paragraphs

Executive and Director Compensation 2 changes

63 unchanged paragraphs

Messrs. Meeter and Raineri s individual 2025 performance was also assessed to be above the target performance level. Accordingly, each of our named executive officers 2025 bonuses was awarded above the target level, resulting in the 2025 bonus payout levels as reported above in the summary compensation table.

Our named executive officers were eligible to earn cash bonuses based on the level of achievement of our 2025 corporate performance goals and their 2025 target bonus amounts. For Messrs. Meeter and Raineri, 2025 bonus eligibility was based on a combination of corporate performance and individual performance, while Dr. McDevitt's McDevitt s 2025 bonus was determined based solely on our corporate performance. Target bonus amounts were set as a percentage of their respective base salaries at 50% for Dr. McDevitt and at 40% for each of Messrs. Meeter and Raineri. For 2025, our corporate performance goals were based on further development of sasineprocel, automated manufacturing initiatives, pipeline strategy, financing, risk mitigation planning and employee engagement goals. Our board of directors determined that we achieved our 2025 corporate performance goals at 109% of the target level. Messrs. Meeter and Raineri s individual 2025 performance was also assessed to be above the target performance level. Accordingly, each of our named executive officers 2025 bonuses was awarded above the target level, resulting in the 2025 bonus payout levels as reported above in the summary compensation table.

68 unchanged paragraphs

Certain Relationships and Related Person Transactions 1 change

24 unchanged paragraphs

We entered into a voting agreement in October 2018, as last amended and restated in October 2025 (Voting Agreement), with the holders of our convertible preferred stock and certain holders of our common stock, including the holders of more than 5% of our capital stock listed above as well as entities with which certain of our directors are affiliated, pursuant to which the following directors were each elected to serve as members on our board of directors and, as of the date of this prospectus, continue to so serve: Caryn Peterson, Peter A. Thompson, M.D., Thomas Daniel, Ph.D., M.D., Douglas Fisher, M.D., Andrew Spaventa, Damien McDevitt, Ph.D., and Faheem Hasnain. Pursuant to the Voting Agreement, Dr. McDevitt, as our Chief Executive Officer, serves on our board of directors as the CEO director. Mr. Spaventa was initially selected to serve on our board of directors as representative of the holders of our common stock, Ms. Peterson was initially selected to serve on our board of directors as representative of the holders of our Series Seed convertible preferred stock, Dr. Thompson and Mr. Daniel were initially selected to serve on our board of directors as representatives of the holders of our Series A convertible preferred stock, and Dr. Fisher was initially selected to serve on our board of directors as a representative of the holders of our Series B convertible preferred stock. Mr. Hasnain was initially selected to serve on our board of directors as the independent director and Chairman of the board of directors.

11 unchanged paragraphs

Principal stockholders 1 change

26 unchanged paragraphs

(5) Consists of (i) shares of our common stock held by ARCH Venture Fund X, L.P. (ARCH X) and (ii) shares of our common stock held by ARCH Venture Fund X Overage, L.P. (ARCH X Overage). A RCH ARCH Venture Partners X, L.P. (AVP X LP), is the sole general partner of ARCH X. ARCH Venture Partners X Overage, L.P. (AVP X Overage LP), is the sole general partner of ARCH X Overage. ARCH Venture Partners X, LLC (AVP X LLC), is the sole general partner of each of AVP X LP and AVP X Overage LP. Keith Crandell, Kristina Burow, Steven Gillis, and Robert Nelsen, collectively the AVP X Committee Members, comprise the investment committee of AVP X LLC. AVP X LP and AVP X Overage LP may be deemed to beneficially own the shares held by ARCH X and ARCH X Overage, respectively, AVP X LLC may be deemed to beneficially own the shares held by ARCH X and ARCH X Overage, and each of the AVP X Committee Members may be deemed to share the power to direct the disposition and vote of the shares held by ARCH X and ARCH X Overage. Each of AVP X LP, AVP X Overage LP, AVP X LLC, and the AVP X Committee Members disclaims beneficial ownership except to any pecuniary interest therein. The address of the ARCH Venture Partners entities is 8755 W. Higgins Road, Suite 1025, Chicago, IL 60631.

11 unchanged paragraphs

Legal Matters 1 change

The validity of the shares of common stock offered hereby will be passed upon for us by DLA Piper LLP (US), San Diego, California. Certain legal matters in connection with this offering will be passed upon for the underwriters are being represented by Latham & Watkins LLP.

Note 7: License Agreements 3 changes

3 unchanged paragraphs

In September 2019, the Company entered into a non-exclusive license agreement with iPS Academia Japan, Inc. ( the AJ License Agreement ) pursuant to which iPS Academia Japan, Inc. granted the Company a license under the licensed patents for the development, manufacture, and sale of licensed products. Pursuant to the AJ License Agreement, the Company is obligated to pay iPS Academia Japan, Inc. an upfront fee of $60,000 and annual maintenance fees of $25,000 until and including the calendar year in which the Company obtains approval of a first new drug application of a licensed product. The Company is obligated to pay future milestone payments up to $0.7 million $135,000 upon the successful achievement of developmental milestones, and up to $1.1 million when certain net sales thresholds of a licensed product are met. The Company is obligated to pay future royalty payments in the low single digit percentage of net sales of licensed products. We will also be subject to an annual minimum royalty of $25,000 following the first approval of a licensed product. The Company recognizes the expense of the milestones when payable.

The AJ License Agreement contains additional customary representations and warranties, covenants, indemnifications and insurance and confidentiality provisions for agreements of its type. The AJ License Agreement may be terminated upon mutual consent of both parties. Unless terminated in accordance with its terms, the AJ License Agreement continues until the expiration, revocation or invalidation of the last patents or the abandonment of the last patent application included within the licensed patents and technology. Payments related to this license agreement are expensed in the period when the contingency is resolved, and the amounts become payable . The Company incurred expenses of $235,000 and $25,000 under this agreement during the years ended December 31, 2025 and 2024.

Payments related to this license agreement are expensed in the period when the contingency is resolved, and the amounts become payable . The Company incurred expenses of $235,000 and $25,000 under this agreement during the years ended December 31, 2025 and 2024.

5 unchanged paragraphs

Undertakings 1 change

11 unchanged paragraphs

Executive Employment Agreement, dated effective as of January 18, 2021, by and between Damien McDevitt and the Registrant 10.10# Employment Offer Letter, dated March 3, 2025, by and between Dalen Meeter and the Registrant 10.11# Employment Offer Letter, dated May 18, 2022, by and between Kim Raineri and the Registrant 10.12#* Form of Indemnification Agreement for Directors and Officers 10.13 * Lease, dated as of March 27, 2019, by and between the Registrant and BMR-Road to the Cure LP 10.14 * First Amendment to Lease, dated as of June 10, 2021, by and between the Registrant and BMR-Road to the Cure LP 10.15 * Second Amendment to Lease, dated as of August 25, 2021, by and between the Registrant and BMR-Road to the Cure LP 10.16 * Third Amendment to Lease, dated as of May 18, 2023, by and between the Registrant and BMR-Road to the Cure LP 10.17 Lease, dated as of May 12, 2021, by and between the Registrant and HCP TPSP, LLC 10.18 * Exclusive License Agreement, dated effective as of July 27, 2018, by and between the Registrant And The Scripps Research Institute and Summit for Stem Cell Foundation 10.19 * Assignment and Assumption Agreement, dated as of October 30, 2018, by and among the Registrant and Summit for Stem Cell Foundation, Mission Edge San Diego 10.20 * Non-Exclusive License Agreement, dated as of September 20, 2019, by and between the Registrant and iPS Academia Japan, Inc. II- 5 10.21 * License Agreement, dated effective as of December 5, 2023, by and between the Registrant and Sumitomo Pharma Co, Ltd. 10.22 * Collaboration and License Agreement, dated as of January 22, 2024, by and between the Registrant and Cell X Technologies, Inc. 10.23 * First Amendment to Collaboration and License Agreement, dated as of January 8, 2025, by and between the Registrant and Cell X Technologies, Inc. 10.24 * Secured Convertible Promissory Note Purchase Agreement, dated as of January 22, 2024, by and between the Registrant and Cell X Technologies, Inc. 10.25* Secured Convertible Promissory Note, dated as of January 22, 2024, by and between the Registrant and Cell X Technologies, Inc. 10.26 * ICON Master Services Agreement, dated as of April 30, 2020, by and between the Registrant and ICON Clinical Research Limited 10.27 * Amendment No. 1 to Master Services Agreement, dated as of April 30, 2025, by and between the Registrant and ICON Clinical Research Limited 10.28* Business Terms and Conditions, dated as of November 12, 2021, by and between the Registrant and Ximedica, LLC (d/b/a Veranex) 10.29* 10.27 Master Supply Agreement, dated as of January 25, 2022, by and between the Registrant and ClearPoint Neuro, Inc. 10.30* 10.28 Main Services Agreement, dated as of September 16, 2024, by and between the Registrant and Mytos Bio Limited 23.1* Consent of Ernst & Young LLP, independent registered public accounting firm 23.2* Consent of DLA Piper LLP (US) (included in Exhibit 5.1) 24.1* Power of Attorney (included on signature page) 107* Filing Fee Table * To be filed by amendment.

15 unchanged paragraphs