Quarterly Report for Quarter Ending June 30, 2026 (Form 10-Q)

Management's Discussion and Analysis of Financial Condition and Results of Operations.

The unaudited interim condensed consolidated financial statements and this Management's Discussion and Analysis of Financial Condition and Results of Operations should be read together with the Notes to Condensed Consolidated Financial Statements included in this Quarterly Report on Form 10-Q and our audited consolidated financial statements and accompanying notes for the year ended December 31, 2025 included in the Annual Report on Form 10-K filed by the Company with the Securities and Exchange Commission (the "SEC") on March 19, 2026 (the "2025 Form 10-K"). In addition to historical information, this discussion and analysis contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Please see Part II, Item 1A. Risk Factors in this Quarterly Report on Form 10-Q for a discussion of certain risk factors applicable to our business, financial condition, and results of operations. Operating results are not necessarily indicative of results that may occur for the full fiscal year or any other future period. See also "Special Note Regarding Forward-Looking Statements" in this Quarterly Report on Form 10-Q. Unless otherwise indicated, references to the terms "Eledon", the "Company", "we", "our", and "us" refer to Eledon Pharmaceuticals, Inc.

ABOUT ELEDON PHARMACEUTICALS

Overview

Eledon is a clinical stage biotechnology company using our immunology expertise in targeting the CD40 Ligand ("CD40L") pathway to develop therapies to protect transplanted organs and prevent rejection, and to treat amyotrophic lateral sclerosis ("ALS"). Our lead compound in development is tegoprubart, an IgG1, anti-CD40L antibody with high affinity for the CD40L, a well-validated biological target that we believe has broad therapeutic potential. We believe the central role of CD40L signaling in both adaptive and innate immune cell activation and function positions it as an attractive target for non-lymphocyte depleting, immunomodulatory therapeutic intervention.

Tegoprubart is engineered to potentially both improve safety and provide pharmacokinetic, pharmacodynamic, and dosing advantages compared to other anti-CD40 approaches. The CD40L/CD40 pathway is recognized for its prominent role in immune regulation. CD40L is primarily expressed on activated CD4+ T cells, platelets and endothelial cells while the CD40 receptor is constitutively expressed on antigen presenting cells such as macrophages and dendritic cells, as well as B cells. By blocking CD40L and not the CD40 receptor, tegoprubart inhibits both the CD40 and CD11 costimulatory signaling pathways, providing the potential for improved efficacy compared to anti-CD40 receptor approaches. Blocking CD40L also increases polarization of CD4+ lymphocytes to Tregs, a specialized subpopulation of T cells that act to suppress an immune response, thus creating a more tolerogenic environment, which may play a therapeutic role in autoimmune diseases and in the prevention of allograft rejection after solid organ transplantation.

Tegoprubart is designed to negate the risk of thrombolytic events seen in the first generation of anti-CD40L antibodies by introducing structural modifications that have been shown in preclinical models to eliminate binding to the Fcγ receptors associated with platelet activation without altering the binding of tegoprubart to CD40L. In non-human primate studies, dosing of tegoprubart up to 200 mg/kg per week for 26 weeks, demonstrated no adverse events regarding coagulation, platelet activation or thromboembolism.

Strategy

Our business strategy is to optimize the clinical and commercial value of tegoprubart and become a global biotechnology company with a focused immunology franchise. Our strategy is to develop tegoprubart for the prevention of rejection of allograft (i.e., transplanting an organ from one human to another) and xenograft (i.e., transplanting an organ from an animal to a human) organs and cells, and for the treatment of ALS. We selected our indications based on preclinical and clinical data that was generated with either tegoprubart or historical anti-CD40L molecules. We remain committed to further progressing ALS clinical development; however, we are unable to continue developing tegoprubart for ALS without additional funding.

Acquisition

In September 2020, we acquired Anelixis Therapeutics, Inc. ("Anelixis"), the company that owned and controlled the intellectual property related to tegoprubart. See Note 7. Commitments and Contingencies of the Notes to Condensed Consolidated Financial Statements included in this Quarterly Report on Form 10-Q for further details of grants and licenses related to this acquisition.

Prior to our acquisition of Anelixis, we focused on developing medicines for patients with disorders of the ear, nose, and throat ("ENT"). In June 2020, we announced that our lead program did not achieve statistical significance for the primary

efficacy endpoints in the treatment of acute otitis media. As a result of this failure to achieve the primary study endpoint, we suspended the clinical development of our legacy ENT assets while we assessed potential development strategies. Following the June 2020 announcement, we significantly curtailed development expenses as we sought to identify strategic alternatives that would maximize stockholder value. As a result of these activities, we acquired Anelixis in September 2020, as described above. After acquiring Anelixis, we terminated our ENT activities and returned our product rights to the original license holders in July 2021.

Clinical Development of Tegoprubart for the Prevention of Allograft Rejection in Kidney Transplantation

In January 2023, we announced plans to prioritize and focus resources on our kidney transplantation programs. We are first focusing on kidney transplantation as this is the most common type of solid organ transplantation in the U.S. with an estimated 270,000 Americans living with a transplanted kidney. There are an estimated 28,000 kidneys transplanted annually in the U.S. Approximately 100,000 people in the U.S. are on a waiting list where they typically wait an average 3-5 years for a kidney transplant while about 5,000 people in the U.S. in need of a kidney transplant die each year waiting for a suitable kidney. Approximately 11% of U.S. people on the waiting list are waiting for a repeat transplant. There remains a critical shortage of kidneys and other organs available for transplantation.

There has been little innovation in immunosuppression therapy for organ transplant patients over the past 30 years. The standard of care immunosuppressive drugs used post-transplant have been shown to reduce the risk of organ rejection, but they are also associated with potentially toxic side effects. Organ transplant recipients require immunosuppression therapy on a lifelong basis, and any disruption in the immunosuppression therapy can trigger transplant rejection. Calcineurin inhibitors ("CNIs") are a critical component of most immunosuppressive regimens for kidney transplants to prevent acute and long-term kidney transplant rejection. However, chronic exposure to CNIs (tacrolimus is the drug most commonly used) is associated with nephrotoxicity, hypertension, new onset diabetes due to pancreatic beta cell toxicity, as well as central nervous system ("CNS") side effects, like tremor. Over time, these CNI side effects may significantly damage the transplanted kidneys or result in a requirement for reduced exposures to CNIs which can lead to an increased risk of rejection. Moreover, CNS side effects like tremors may result in patients decreasing their adherence to their medicines. Today, an implanted kidney is expected to fail within 10-15 years on average using currently available immunosuppression options. The fact that American transplant patients are on average in their 50s means that many of them will ultimately need a second or even third transplant procedure during their lifetime or a return to dialysis.

The central role of CD40L signaling in generating pro-inflammatory responses makes it a highly attractive candidate for therapeutic intervention in the protection of transplanted organs and prevention of transplant rejection. Results from prior studies demonstrate that targeting and blocking CD40L has the potential for better efficacy and improved safety, including reduced risk of nephrotoxicity, diabetes, hypertension, and other side effects associated with standard-of-care CNIs such as tacrolimus.

Tegoprubart seeks to address challenges associated with current immunosuppressive transplantation regimens using CNI-based therapies. The ability to prevent acute and chronic transplant rejection without the need for CNIs has the potential to transform the clinical management of preventing graft rejection by mitigating the adverse events associated with CNIs and improving long-term graft survival, thus potentially decreasing the need for repeat kidney transplants and increasing organ availability for other patients on the wait list. By identifying and advancing novel strategies in immunosuppression including targeting the CD40L pathway, we may be able to help organs remain functional for longer and potentially throughout the natural lifespan of each recipient.

Phase 1b Clinical Trial

We have received regulatory approvals in the United States, Canada, the United Kingdom and Australia, for a Phase 1b clinical trial of tegoprubart in up to 36 subjects, replacing tacrolimus as an immunosuppressive regimen component in patients undergoing de novo kidney transplantation. Each participant receives rabbit antithymocyte globulin induction and a maintenance regimen consisting of tegoprubart, mycophenolate mofetil, and corticosteroids. The primary endpoint of the study is safety. Other endpoints include estimated glomerular filtration rate ("eGFR"), characterizing the pharmacokinetic profile of tegoprubart, and the incidence of biopsy-proven rejection.

Better graft function as assessed by eGFR has been associated with improved long-term patient and graft survival and is an early predictor of future graft failure. Historical studies have reported average eGFRs generally in the low 50

mL/min/1.73 m2 range during the first year after kidney transplant using current standard of care immunosuppression. An eGFR of 60 mL/min/1.73 m2 or below generally indicates chronic kidney disease.

The first subject in the Phase 1b study was dosed in July 2022. We reported interim safety and efficacy results from the Phase 1b clinical trial in March 2023, and provided updated data in November 2023, June 2024 and August 2025.

At the time of the August 2025 update, which reported data as of July 2025, 32 patients undergoing kidney transplantation were enrolled in the Phase 1b study. The updated data showed that kidney function, as assessed by eGFR, stabilized after the first month post-transplant and remained in the range of approximately 68 mL/min/1.73 m2 through 12 months for patients (n = 12) who remained on tegoprubart. Kidney function in the intention-to-treat population (n=15) was approximately 63 mL/min/1.73 m2 at 12 months. Data from historical studies using the standard of care, CNI-based immunosuppression therapy, typically report aggregate mean eGFR of approximately 53 mL/min/1.73 m2 during the first year after kidney transplant. In addition, preliminary abbreviated iBox data was presented suggesting that tegoprubart may improve 5-year graft survival. Abbreviated iBox, a composite biomarker panel developed by the Paris Transplant Group, incorporates kidney function (eGFR, proteinuria) and immunologic response (donor-specific HLA antibodies) parameters into a single prognostic score. Based on data collected as of July 2025, abbreviated iBox scores were -3.75 in the intention-to-treat population and -4.11 in the on-treatment population, which compare favorably to a -2.98 historical mean for CNIs. A difference in abbreviated iBox score of -0.40 at 12 months is considered predictive of a 4-5% difference in 5-year graft survival suggesting that tegoprubart may have a predicted 5-year allograft survival rate of over 96%. As of July 2025, there were six (18.8%) rejection episodes, and 75% of patients who experienced a rejection had received low-dose rabbit antithymocyte globulin induction. All rejection episodes were successfully treated. Of the patients who experienced a rejection episode and completed a year in the study, three who remained on tegoprubart had a mean eGFR of approximately 73 mL/min/1.73 m2 at 12 months, indicating full recovery of kidney function, while the two patients who switched to standard of care tacrolimus had a mean eGFR of approximately 34 mL/min/1.73 m² at 12 months.

In January 2026, we presented 24-month data from eight patients enrolled in the Phase 1b trial long-term extension evaluating tegoprubart in kidney transplantation at the American Society of Transplant Surgeons Winter Symposium held in Scottsdale, Arizona. During the reported follow-up period, no episodes of biopsy-proven acute rejection, graft loss, death, new-onset diabetes mellitus, or de novo donor-specific antibody formation were observed among participating patients. Mean eGFR increased over the measurement period from 67.0 mL/min/1.73 m² at 12 months to 74.2 mL/min/1.73 m² at 24 months.

Phase 2 BESTOW Trial

In July 2022, we received Investigational New Drug ("IND") application clearance from the FDA for our controlled, Phase 2 BESTOW trial of tegoprubart for the prevention of transplant rejection in persons receiving a kidney transplant. The BESTOW study is a multi-center, two-arm, active comparator, head-to-head superiority clinical study, with approximately 120 participants undergoing kidney transplantation in the U.S. and other countries to evaluate the safety, pharmacokinetics, and efficacy of tegoprubart compared to the calcineurin inhibitor tacrolimus. The study's primary objective is to assess graft function as measured by eGFR at 12 months post-transplant in participants treated with tegoprubart compared to tacrolimus. Secondary objectives are the assessment of graft survival, biopsy-proven acute rejection, and the incidence of new onset diabetes mellitus after transplant. The BESTOW study is running in parallel to the ongoing Phase 1b clinical trial of tegoprubart in kidney transplantation. The first subject in the BESTOW study was dosed in August 2023 and the last patient was dosed on September 4, 2025.

On November 6, 2025, we announced topline efficacy and safety data for 12-months post transplant from the Phase 2 BESTOW trial evaluating tegoprubart for the prevention of kidney transplant rejection. Safety and efficacy results supported the potential for tegoprubart to provide effective immunosuppression with a favorable safety and tolerability profile compared to tacrolimus. Safety findings underscore tegoprubart's potential to maintain effective immunosuppression while minimizing the metabolic, neurologic, and cardiovascular toxicities characteristic of tacrolimus-based therapy. Notably, new-onset diabetes developed in approximately 17% of patients receiving tacrolimus versus 2% receiving tegoprubart. Tremor was markedly higher in the tacrolimus group (25.0% vs. 1.6%) and cardiovascular effects, including hypertension (25.0% vs. 15.9%), hypertensive crisis (7.8% vs. 1.6%), and heart failure (4.7% vs. 0%) all favored tegoprubart. Delayed graft function occurred less often with tegoprubart and required shorter dialysis (14.3% vs. 25%; 4.6 days vs. 6.1 days) suggesting potential reductions of 115 days on dialysis post-transplant per 100 deceased donor kidney recipients on tegoprubart versus tacrolimus. Sepsis or bacteremia occurred more frequently in the tacrolimus arm (17.2% vs. 4.8%) and viral infection rates (CMV, BK, EBV, fungal) were similar across groups, with no cases of Post-Transplant Lymphoproliferative Disorder or Progressive Multifocal Leukoencephalopathy. Additionally, overall rates of serious adverse events were comparable between treatment arms. From an efficacy standpoint, tegoprubart achieved an eGFR of approximately 69 mL/min/1.73 m² (n=51) at 12 months compared to 66 mL/min/1.73 m² for tacrolimus (n=56). Although the primary endpoint did not reach statistical significance,

tegoprubart maintained strong renal function, delivering what the Company believes is one of the highest mean eGFR levels reported to date in kidney transplant clinical trials evaluating rejection prevention. Subgroup analyses showed higher eGFRs in nearly all tegoprubart subgroups compared to tacrolimus, particularly among living-related donor recipients (72 mL/min/1.73 m² vs. 62 mL/min/1.73 m²) and high Kidney Donor Profile Index (KDPI > 35) transplants (62 mL/min/1.73 m² vs. 53 mL/min/1.73 m²). The efficacy failure composite endpoint, comprising death, graft loss and biopsy proven acute rejection, is the approval endpoint historically recognized by the FDA. The efficacy failure composite endpoint was 22% in the tegoprubart group versus 17% in the tacrolimus group, demonstrating non-inferiority for tegoprubart versus tacrolimus, using a 20% non-inferiority margin. We believe these results, if replicated in a Phase 3 study, would be sufficient to support tegoprubart's approvability. The rate of acute rejection in all biopsies was 20.6% for tegoprubart group compared with 14.1% in the tacrolimus group. Among patients in the tegoprubart group who experienced acute rejection and remained on treatment through month 12, mean eGFR was 73 mL/min/1.73 m² compared to 50 mL/min/1.73 m² in those who switched to tacrolimus. Additionally, there was one case of donor-specific antibodies in the tegoprubart arm versus two in the tacrolimus arm.

Phase 2 Open-Label Extension Study

In October 2023, we enrolled the first participant in a Phase 2 open-label extension study which is designed to evaluate the long-term safety, pharmacokinetics, and efficacy of tegoprubart in participants who have completed one year of treatment in either the ongoing Phase 1b study or the Phase 2 BESTOW study.

In June 2026, we announced new long-term data from our Phase 2 BESTOW clinical program evaluating tegoprubart for the prevention of kidney transplant rejection, including updated results from the Phase 2 BESTOW trial and new long-term follow-up data from the BESTOW long-term extension study. Among patients who completed 12 months of treatment in the BESTOW trial, 96% (49/51) of tegoprubart-treated patients and 86% (48/56) of tacrolimus-treated patients enrolled in the long-term extension study. As of the data cutoff, mean follow-up was 21 months, with 89 patients followed through 18 months, 20 patients followed through 24 months, and the longest-followed ongoing patient followed for approximately 33 months. Kidney graft function, as assessed by eGFR, stabilized after the first month of treatment and remained higher in tegoprubart-treated patients than in tacrolimus-treated patients at each reported time point. At month 18, tegoprubart-treated patients demonstrated a statistically significant, approximately 12 mL/min/1.73 m² higher mean eGFR compared to tacrolimus-treated patients (74 vs. 61 mL/min/1.73 m²; p<0.05). No biopsy-proven acute rejection (BPAR) events were observed in tegoprubart-treated patients after the first six months of treatment, whereas in the tacrolimus arm, seven of 11 total BPAR events (approximately 64%) occurred after six months, including two events after 12 months: one new case of active antibody-mediated rejection (aAMR) and one recurrent case of active T-cell-mediated rejection with aAMR. In an exploratory analysis of patients who experienced rejection following transplantation, those who remained on tegoprubart maintained higher mean eGFR than tacrolimus-treated patients who experienced rejection, with the observed difference increasing from approximately 15 mL/min/1.73 m² at 12 months to approximately 25 mL/min/1.73 m² at 21 months. Patient-reported outcome measures demonstrated lower symptom burden among tegoprubart-treated patients compared to tacrolimus-treated patients at 52 weeks, with statistically significant improvements on the Modified Transplant Symptom Occurrence and Symptom Distress Scale (MTSOSD-59R; treatment difference: -12.2; 95% CI: -19.7, -4.6; p<0.05) and the KDQOL-36 Symptoms and Problems domain (treatment difference: 5.7; 95% CI: 1.0, 10.5; p<0.05). Long-term follow-up from our Phase 1b study for patients treated at the 20 mg/kg dose of tegoprubart was consistent with the Phase 2 BESTOW results, with no BPAR episodes observed after six months in tegoprubart-treated patients. From a safety perspective, key central nervous system and kidney-related adverse events in the long-term extension study were observed more frequently in the tacrolimus arm than in the tegoprubart arm, including headache (12% vs. 2%), extremity pain (10% vs. 0%), fall or loss of balance (6% vs. 0%), acute kidney injury (6% vs. 2%), and diarrhea (21% vs. 10%). No graft loss, PML, PTLD, BK or CMV nephropathy/disease, or new malignancies were reported in the long-term extension study, and no new proteinuria was reported in the tegoprubart arm. One death occurred in the tegoprubart arm and was not attributed to the study drug.

Phase 3 Planning

In the second quarter of 2026, we held an End-of-Phase 2 meeting with the FDA, and following that meeting we have established the regulatory framework for our Phase 3 kidney transplantation program and plan to initiate Phase 3 clinical development of tegoprubart in late 2026. We expect the Phase 3 primary endpoint to be non-inferiority versus tacrolimus at 52 weeks on a composite of BPAR, graft loss and death. The Phase 3 study is expected to incorporate key learnings from the Phase 2 BESTOW trial and ongoing long-term extension study. We will need to raise additional financing to initiate a Phase 3 clinical trial in kidney transplantation. There can be no assurance such financing will be available to us on acceptable terms, or at all, for this trial, which could force us to significantly alter our business strategy, substantially curtail our current operations, or liquidate and cease operations altogether.

Clinical Development of Tegoprubart for the Prevention of Allograft Rejection in Xenotransplantation

While inhibition of CD40L has shown it may play an important role in immunosuppression in allograft kidney transplantation, this mechanism of action has also demonstrated that it may be a promising option in xenotransplantation (i.e., transplanting an organ from an animal to a human).

In January 2023, we entered into a non-exclusive collaborative research agreement with eGenesis, Inc., ("eGenesis"), under which eGenesis gained access to tegoprubart for preclinical and clinical xenotransplantation studies in support of eGenesis' kidney, heart and islet cell xenotransplantation programs.

To date, tegoprubart has been used as a key component of the immunosuppression regimen in four xenotransplantation procedures: three involving genetically modified pig kidneys and one involving a genetically modified pig heart. Two of the kidney transplant recipients remain alive. One continues to maintain kidney function with the transplanted pig kidney, while the other had the graft removed on day 271 and has since received an allograft kidney from a donor.

We expect to continue discussions with regulatory authorities regarding the potential path to market for tegoprubart in xenotransplantation.

Clinical Development of Tegoprubart for the Prevention of Allograft Rejection in Islet Cell Transplantation ("ICT")

Type 1 diabetes ("T1D") is a T cell mediated autoimmune disease with progressive loss of insulin producing pancreatic beta cells and affects approximately 2 million persons in the United States. Approximately 33% of people with T1D report impaired awareness of hypoglycemia regardless of continuous glucose monitoring or automated insulin usage. Approximately 12% of people with T1D experience recurrent severe hypoglycemic episodes annually, putting them at higher risk for adverse outcomes such as seizures, coma, and death. ICT is gaining attention as a therapeutic option for T1D because it can restore physiological insulin secretion, minimize the risk of hypoglycemic unawareness, and reduce the risk of death due to severe hypoglycemia. The advances made in this field over the past decade have improved patient outcomes, and the procedure has been evolving from an experimental treatment to a clinical treatment option.

A number of issues are believed to continue to hamper the overall success of ICT and to need to be addressed in order for there to be widespread clinical acceptance. These include the acute loss of transplanted islets with current immunosuppressive treatments, particularly those with CNI-based therapies, due to islet cell toxicity and alloreactive immunologic responses to transplanted islets. Over time, the progressive loss of islet cells and decline in islet cell function can lead to the need for multiple transplants in order for T1D patients to have optimal response to blood glucose levels and possibly achieve insulin independence. Tegoprubart seeks to address the challenges associated with current ICT immunosuppressive regimens using CNI-based therapies, by replacing the CNIs with tegoprubart to prevent rejection and protect the transplanted cells. We believe that tegoprubart may unlock the ICT market by potentially improving islet cell graft survival and reduce the side effects associated with standard of care regimens.

Historical studies in nonhuman primate models of ICT have demonstrated that treatment with anti-CD40L antibodies induces long term islet cell function and graft survival, even as a monotherapy. Tegoprubart has shown pre-clinical, proof-of-concept efficacy in a non-human primate model of T1D, where animals undergoing ICT maintained glucose control and sustained levels of C-peptide with chronic tegoprubart treatment for up to a year. Compared to combination immunosuppressive therapy including CNIs, tegoprubart monotherapy was more effective in preventing long term islet cell rejection, associated with better graft function, and showed an improved safety profile.

In 2022, the FDA granted orphan drug designation to tegoprubart for the prevention of allograft rejection in pancreatic islet cell transplantation.

In January 2024, we announced that tegoprubart would be evaluated in an investigator-initiated clinical trial conducted at the University of Chicago Medicine's Transplant Institute. The study is designed to assess the safety of a CNI-free immunosuppression regimen utilizing tegoprubart in individuals with T1D mellitus undergoing islet cell transplantation. We are not funding the trial and our involvement is limited to supplying tegoprubart for use in the study.

As of March 2026, updated data from this investigator-initiated clinical trial included 12 adults with long-standing T1D undergoing allogeneic islet transplantation at University of Chicago Medicine. Among the 10 patients with more than four weeks of follow-up, all achieved insulin independence with a most recent hemoglobin A1c ("HbA1c") below 6.0% and a mean most recent HbA1c of approximately 5.35%. Tegoprubart, administered as part of a CNI-free immunosuppression

regimen, was generally well tolerated, with no rejection episodes, no de novo donor-specific HLA antibodies, and no evidence of nephrotoxicity, hypertension, or neurotoxicity observed during the reported follow-up period.

In June 2026, we announced further updated results from this investigator-initiated trial. All 12 adults enrolled in the trial showed stable islet graft function over a median and maximum post-transplant follow-up period of 8 and 22 months, respectively. All 12 patients continued to achieve insulin independence, meaning they no longer required chronic, exogenous insulin therapy to manage their T1D, and all patients demonstrated a most recent HbA1c below the diabetic threshold of 6.5%, with a mean most recent HbA1c of approximately 5.4% across the cohort. While all enrolled patients reported recurrent severe hypoglycemic events prior to transplantation, no severe hypoglycemic episodes were reported following transplantation. Higher levels of post-transplant islet cell engraftment were observed with the tegoprubart-based immunosuppression regimen than in historical patients treated with a tacrolimus-based immunosuppression regimen at the same center. There were no rejection episodes, and no patients developed de novo donor-specific HLA antibodies. Tegoprubart-based immunosuppression was generally well tolerated, with immunosuppression-related adverse events generally successfully treated by lowering the mycophenolic acid dose, if necessary, and no evidence of nephrotoxicity, hypertension, or neurotoxicity, which are commonly associated with CNI-based immunosuppression regimens, was observed. We believe these findings further support the potential of CD40L blockade to enable effective islet graft protection while avoiding the toxicities of CNIs such as tacrolimus.

Following our interactions with the FDA, we are advancing our plans to launch a registrational path study for tegoprubart in islet cell transplantation. We will need to raise additional financing to initiate registrational studies in islet cell transplantation. There can be no assurance such financing will be available to us on acceptable terms, or at all, for these studies, which could force us to significantly alter our business strategy, substantially curtail our current operations, or liquidate and cease operations altogether.

Clinical Development of Tegoprubart for the Prevention of Allograft Rejection in Liver Transplantation

In March 2026, the FDA granted orphan drug designation to tegoprubart for the prevention of allograft rejection in liver transplantation, the third orphan drug designation received by tegoprubart from the FDA.

We plan to initiate an investigator-led study evaluating tegoprubart for the prevention of allograft rejection in patients receiving a de novo liver transplant.

Clinical Development of Tegoprubart for ALS

ALS is a progressive, paralytic disorder characterized by degeneration of motor neurons in the brain and spinal cord. In the U.S., the incidence is estimated at approximately 5,000 cases per year with a prevalence of approximately 30,000 cases overall. Despite 3 approved drugs, in most cases, death from respiratory failure occurs between 3 to 5 years from diagnosis, with 50% of patients living at least 3 years from diagnosis and only 20% of patients living at least 5 years from diagnosis.

While the exact pathogenic mechanism of ALS is still not fully understood, there is strong evidence indicating that neuroinflammation plays an important role in the disease's pathogenesis. Neuroinflammation in ALS is characterized by the infiltration of lymphocytes and macrophages into the central nervous system, and the activation of microglia and reactive astrocytes. Reactive astrocytes and microglia as well as infiltrating lymphocytes, dendritic cells, monocytes, macrophages and immune complexes have been identified in cerebrospinal fluid and neural tissues in both animal models of ALS and at autopsy in ALS patients.

Tegoprubart is designed to block CD40L binding to CD40, thereby potentially inhibiting neuroinflammatory pathways leading to disease progression in ALS. In vitro proof-of-concept studies have shown that tegoprubart binds to CD40L in human cells and blocks the CD40L binding on antigen presenting cells and activated T cells. The potential for therapeutic benefit of CD40L blockage in treating ALS has been demonstrated in a SOD1 mouse model of ALS, where a murine anti-CD40L antibody prolonged survival and delayed the onset of neurological disease progression. These pathophysiological manifestations are believed to be due to reduced immune cell infiltration of macrophages into skeletal muscle and their destroying denervated nerves. The plasticity of the nervous system to repair itself in the absence of this immune cell attack is believed to result in improved neuromuscular junction occupancy and improved muscle function. Blocking CD40L signaling also prevents pro-inflammatory polarization of lymphocytes, reduced neuroinflammation and improved motor neuron survival in rodent ALS models.

In 2018, the FDA granted orphan drug designation to tegoprubart for ALS. In 2019, we completed a single ascending dose Phase 1 study of tegoprubart in healthy volunteers and people with ALS. In this study, the doses of tegoprubart studied

were well tolerated in healthy adult subjects and adults with ALS. Tegoprubart demonstrated low anti-drug antibody responses that were not dose related, linear dose proportionality across the dose ranges, and a half-life of up to 26 days.

In October 2020, we initiated a Phase 2a, open-label, multi-center study to evaluate the safety and tolerability of multiple doses of tegoprubart in adult subjects with ALS. Fifty-four subjects with ALS were enrolled into the study in the United States and Canada at 13 ALS treatment sites. Ascending doses of tegoprubart were administered as IV infusions to four sequentially enrolling cohorts. The first two cohorts consisted of nine participants, and the last two cohorts of 18 participants each. All enrolled subjects received six infusions of tegoprubart over a 12 week period. Blood samples for target engagement, and exploratory biomarkers for inflammation and neurodegeneration were taken and analyzed. Participant-focused clinical outcomes were also assessed. In May 2022, we completed the Phase 2a study and released positive topline results. Tegoprubart successfully met the primary endpoints of safety and tolerability. Fifty of the fifty-four subjects completed all six study infusions, and adverse events were typical of an ALS patient population. Tegoprubart was well-tolerated, and no drug-related serious adverse events were observed. No new safety signals emerged. Anti-drug antibodies ("ADAs") were present in less than 5 percent of samples. All ADAs were of low titer and did not impact tegoprubart drug levels. Tegoprubart target engagement was demonstrated in all dose cohorts with increasing target engagement in a dose-dependent manner, plateauing at the 4 and 8 mg / kg dosing levels using CD40L and CXCL13 biomarkers related to T cell and B cell function, respectively. Tegoprubart exposure decreased inflammatory biomarker levels, in a dose dependent manner, in 20 of 32 pro-inflammatory proteins. Pro-inflammatory biomarkers reduced included biomarkers also associated with IgA nephropathy and kidney transplant rejection, such as IgA, IgE, IgM, C3, CXCL9, and CXCL10.

We are seeking to further progress ALS clinical development; however, we will be unable to continue this program without additional financing dedicated to ALS, and we can provide no assurance that such financing will be available on acceptable terms, or at all.

Clinical Development of Tegoprubart for IgA Nephropathy

In January 2023, the Company announced the deprioritization of its IgAN program and all IgAN clinical development activities were discontinued in 2023. IgAN is the leading cause of chronic glomerulonephritis, a state of inflammation producing damage to the filtering part of the kidney. Disease manifestation and clinical presentation involves renal dysfunction characterized by proteinuria with a slow relentless course. Approximately 30%-40% of persons living with IgAN ultimately reach end stage renal disease ("ESRD"). The standard of care for ESRD is dialysis or kidney transplant, which represents a significant economic burden as well as a major impact on a patient's quality of life. With an estimated prevalence of approximately 150,000 persons in the United States, IgAN is one of the most common autoimmune glomerulonephropathies. In the United States, oral budesonide Tarpeyo was approved for use in IgAN by the FDA in December 2021 and Kinpeygo received conditional approval by the European Medicines Agency ("EMA") in July 2022.

In August 2022, we received IND clearance from the FDA to evaluate tegoprubart for the treatment of IgAN. The Phase 2 global study was a 96-week open-label, dose ranging trial, and included both a high dose and a low dose cohort. The primary endpoint was change in urinary protein:creatinine ratio at week twenty-four. Secondary endpoints included change in eGFR at week 96 as well as safety and tolerability. The first subject was dosed in May 2022. We reported interim safety data from the Phase 2 high dose cohort in March 2023.

Financing Activities

2024 Equity Distribution Agreement

On September 20, 2024, the Company entered into an Open Market Sale Agreement (the "Sales Agreement") with Guggenheim Securities, LLC ("Guggenheim Securities") to sell shares of the Company's common stock, having aggregate sales proceeds of up to $75.0 million, from time to time, through an "at-the-market" equity offering program under which Guggenheim Securities will act as sales agent. In connection with the Sales Agreement, the Company filed on September 20, 2024 a registration statement on Form S-3 containing a prospectus and prospectus supplement (the "Initial Shelf Registration Statement") with the SEC. The Initial Shelf Registration Statement became effective on October 2, 2024. In advance of the expiration of the Initial Shelf Registration Statement, the Company filed on May 1, 2026 a new registration statement on Form S-3 containing a prospectus and prospectus supplement with the SEC, which became effective on May 11, 2026 and replaces the Initial Shelf Registration Statement. As of June 30, 2026, we have not sold any shares under the Sales Agreement.

2025 Underwritten Offering

On November 12, 2025, the Company entered into an underwriting agreement (the "Underwriting Agreement") with Leerink Partners, LLC, as representative of the several underwriters named therein (the "Underwriters"), in connection with the underwritten public offering and sale by the Company (the "2025 Underwritten Offering") of 15,152,485 shares of the Company's common stock at a public offering price of $1.65 per share (the "Common Stock Purchase Price"), and pre-funded warrants (the "2025 Offering Pre-Funded Warrants") at a public offering price of $1.649 per 2025 Offering Pre-Funded Warrant, which are exercisable to purchase up to 15,151,515 shares of common stock at an exercise price of $0.001 per share. In addition, pursuant to the Underwriting Agreement, the Company granted the Underwriters an option (the "Option"), exercisable for 30 days, to purchase up to 4,545,600 additional shares of common stock at the Common Stock Purchase Price less the underwriting discounts and commissions, which Option was exercised in full by the Underwriters.

The 2025 Underwritten Offering closed on November 13, 2025 and resulted in gross proceeds of $57.5 million or net proceeds of approximately $53.6 million after deducting the underwriting discounts and commissions and offering expenses. The 2025 Underwritten Offering was made pursuant to the Initial Shelf Registration Statement and a prospectus supplement relating to the 2025 Underwritten Offering dated November 12, 2025.

A holder of the 2025 Offering Pre-Funded Warrants (together with its affiliates) may not exercise any portion of a 2025 Offering Pre-Funded Warrant to the extent that, after giving effect to such exercise, the holder (together with the holder's affiliates, and any other persons acting as a group together with the holder or any of the holder's affiliates) would beneficially own in excess of 4.99% of the number of shares of the Company's common stock outstanding immediately after giving effect to the issuance of shares of common stock issuable upon exercise of such 2025 Offering Pre-Funded Warrant. A holder, upon notice to the Company, may increase or decrease such beneficial ownership limitation, provided that in no event shall the limitation exceed 19.99% of the number of shares of the common stock outstanding immediately after giving effect to the issuance of shares of common stock upon exercise of the 2025 Offering Pre-Funded Warrant.

2025 Warrant Exchange Agreement

On December 30, 2025, the Company entered into an exchange agreement (the "Warrant Exchange Agreement") with Coastlands Capital Partners LP ("Coastlands Capital"), pursuant to which Coastlands Capital agreed to exchange 4,203,764 shares of the Company's common stock for a pre-funded warrant to purchase an aggregate of 4,203,764 shares of the Company's common stock (the "Exchange Warrant"), and the Company cancelled the 4,203,764 shares of common stock delivered in the exchange.

Coastlands Capital (together with its affiliates) may not exercise any portion of the Exchange Warrant to the extent that, after giving effect to such exercise, Coastlands Capital (together with its affiliates and any other persons acting as a group together with Coastlands Capital or any of its affiliates) would beneficially own in excess of 4.99% of the number of shares of the Company's common stock outstanding immediately after giving effect to the issuance of shares of common stock issuable upon exercise of the Exchange Warrant. Coastlands Capital may increase or decrease such beneficial ownership limitation, provided that in no event shall the limitation exceed 19.99% of the number of shares of the common stock outstanding immediately after giving effect to the issuance of shares of common stock upon exercise of the Exchange Warrant.

On June 4, 2026, the Company issued 2,999,138 shares of its common stock to Coastlands Capital Partners LP upon the cashless exercise of 3,000,000 pre-funded warrants in accordance with the terms of the pre-funded warrant issued pursuant to the Warrant Exchange Agreement. The exercise did not result in any cash proceeds to the Company.

Common Stock Warrants, Convertible Preferred Stock and Pre-Funded Warrants

As of June 30, 2026, common stock warrants were exercisable into an aggregate of 15,151,518 shares of common stock (after rounding for fractional shares and subject to beneficial ownership conversion blockers) at an exercise price of $3.00 per share. These warrants expire on May 5, 2028. The shares of common stock underlying the common stock warrants are registered for offer and sale under the Securities Act pursuant to our effective registration statements on Forms S-3.

On April 9, 2026, the Company issued an aggregate of 1,248,832 shares of its common stock upon the conversion of an aggregate of 22,479 shares of its Series X1 non-voting convertible preferred stock held by Biotechnology Value Fund, L.P., Biotechnology Value Fund II, L.P., Biotechnology Value Trading Fund OS LP and MSI BVF SPV, LLC, in accordance with the Certificate of Designation of Preferences, Rights and Limitations of the Series X1 non-voting convertible preferred stock. The conversion did not result in any cash proceeds to the Company.

On April 10, 2026, the Company issued 87,269 shares of its common stock to MSI BVF SPV, LLC upon the cashless exercise of 87,300 pre-funded warrants in accordance with the terms of the pre-funded warrants issued pursuant to the underwriting agreement, dated October 29, 2024, by and between the Company and Leerink Partners, LLC, as representative of the several underwriters named therein. The exercise did not result in any cash proceeds to the Company.

On June 30, 2026, the Company issued an aggregate of 655,943 shares of its common stock upon the conversion of an aggregate of 11,807 shares of its Series X1 non-voting convertible preferred stock held by Biotechnology Value Fund, L.P., Biotechnology Value Fund II, L.P., Biotechnology Value Trading Fund OS LP and MSI BVF SPV, LLC, in accordance with the Certificate of Designation of Preferences, Rights and Limitations of the Series X1 non-voting convertible preferred stock. The conversion did not result in any cash proceeds to the Company.

Financial Operations Overview

Operating Expenses

Our operating expenses consist primarily of costs associated with research and development activities and general and administrative activities.

Research and Development Expenses

Research and development expenses, which consist primarily of costs associated with our product research and development efforts, are expensed as incurred. Research and development expenses consist primarily of:

General and Administrative Expenses

General and administrative expenses consist primarily of personnel costs that include salaries, benefits and travel expenses for our executive, finance, and other administrative functions, and stock-based compensation expense. General and administrative expenses also include professional fees for expenses incurred under agreements with third parties relating to public relations, audit, tax and legal services, including legal expenses to pursue patent protection of our intellectual property; and our information technology, facilities and other related expenses, including rent, maintenance of facilities, insurance and supplies.

Change in fair value of warrant liabilities

Change in fair value of warrant liabilities represents the initial recognition of warrant liabilities at fair value in excess of proceeds received, as well as subsequent period remeasurements of these warrant liabilities at fair value. These remeasurements reflect changes in market conditions, such as fluctuations in stock price, volatility, interest rates, and other valuation inputs that impact the fair value of the liability.

CRITICAL ACCOUNTING ESTIMATES

Our management's discussion and analysis of our financial condition and results of operations are based on our condensed consolidated financial statements, which have been prepared in accordance with accounting principles generally accepted in the United States ("GAAP"). The preparation of these financial statements requires us to make estimates and judgments that affect the reported amount of assets, liabilities, and expenses and the disclosure of contingent assets and

liabilities as of the date of the financial statements. On an ongoing basis, we evaluate our estimates and judgments. We base our estimates on historical experience, known trends and events, and various other factors that are believed to be reasonable under the circumstances, the results of which form the basis for making judgments about the carrying value of assets and liabilities that are not readily apparent from other sources. Actual results may differ materially from these estimates under different assumptions or conditions. In Part II, Item 7 of the 2025 Form 10-K, we disclosed our critical accounting estimates, which are those estimates made in accordance with GAAP that involve a significant level of estimation uncertainty and have had or are reasonably likely to have a material impact on our financial condition or results of operation. There have been no significant changes in our critical accounting estimates during the six months ended June 30, 2026, as compared to those disclosed in the 2025 Form 10-K.

Recently Issued Accounting Pronouncements

A description of recently issued accounting pronouncements that may potentially impact our financial position and results of operations is set forth in Note 2. Summary of Significant Accounting Policies, of the Notes to Condensed Consolidated Financial Statements included in this Quarterly Report on Form 10-Q.

Market Trends and Uncertainties

The global economy, including the financial and credit markets, has recently experienced extreme volatility and disruptions, including severely diminished liquidity and credit availability, declines in consumer confidence, declines in economic growth, increases in unemployment rates, elevated inflation and interest rates, changes in U.S. trade policy and uncertainty about economic stability. Likewise, the current conflicts in Ukraine and the Middle East have created volatility in the global capital markets and global economic consequences, including disruptions of the global supply chain and energy markets. A severe or prolonged economic downturn or continued volatility in the financial and credit markets could negatively impact our ability to obtain necessary debt or equity financing in a timely manner or on favorable terms, if at all. The severity and duration of any such impacts cannot be predicted. Any such failure to raise capital as and when needed could have a negative impact on our financial condition and on our ability to pursue our business plans and strategies or cause us to delay our clinical development plans, research and development programs or commercialization efforts, out-license intellectual property rights to our product candidates or sell unsecured assets, or a combination of the above. Any of these actions could materially harm our business.

Any of the foregoing items could materially affect our business, possibly to a significant degree. The severity and duration of any such impacts cannot be predicted. See Item 1A. "Risk Factors" in Part II of this Quarterly Report on Form 10-Q for additional information.

RESULTS OF OPERATIONS

Comparison of the Three Months Ended June 30, 2026 and 2025

The following table provides comparative unaudited results of operations for the three months ended June 30, 2026 and 2025 (in thousands):

Research and Development Expenses

The following table summarizes the period-over-period changes in research and development expenses for the periods presented (in thousands):

Research and development expenses decreased $2.0 million for the three months ended June 30, 2026, compared to the three months ended June 30, 2025. The decrease was primarily attributable to the following:

General and Administrative Expenses

The following table summarizes the period-over-period changes in general and administrative expenses for the periods presented (in thousands):

General and administrative expenses increased by $0.2 million for the three months ended June 30, 2026, compared to the three months ended June 30, 2025. The increase was primarily attributable to the following:

Other Income, Net

Other income, net for the three months ended June 30, 2026 decreased by $0.4 million compared to the three months ended June 30, 2025, primarily due to lower interest rates and lower average balances of cash, cash equivalents, and short-term investments.

Change in Fair Value of Warrant Liabilities

For the three months ended June 30, 2026, the fair value of warrant liabilities increased by $9.6 million. This change was primarily driven by an increase in the fair value of the Common Warrants, reflecting an increase in the Company's stock price during the period.

By comparison, for the three months ended June 30, 2025, the fair value of the warrant liabilities decreased by $12.3 million, primarily due to a decline in the Company's stock price during the period.

Comparison of the Six Months Ended June 30, 2026 and 2025

The following table provides comparative unaudited results of operations for the six months ended June 30, 2026 and 2025 (in thousands):

Research and Development Expenses

The following table summarizes the period-over-period changes in research and development expenses for the periods presented (in thousands):

Research and development expenses increased $1.6 million for the six months ended June 30, 2026, compared to the six months ended June 30, 2025. The increase was primarily attributable to the following:

General and Administrative Expenses

The following table summarizes the period-over-period changes in general and administrative expenses for the periods presented (in thousands):

General and administrative expenses decreased by $0.3 million for the six months ended June 30, 2026, compared to the six months ended June 30, 2025. The decrease was primarily attributable to the following:

Other Income, Net

The $0.7 million decrease in other income, net for the six months ended June 30, 2026 compared to the six months ended June 30, 2025, was primarily due to a decrease in interest income, reflecting lower interest rates and lower average balances of cash, cash equivalents, and short-term investments.

Change in Fair Value of Warrant Liabilities

For the six months ended June 30, 2026, the fair value of warrant liabilities increased by $28.6 million. This change was primarily driven by an increase in the fair value of the Common Warrants, reflecting an increase in the Company's stock price during the period. The warrant liability increased from $11.4 million as of December 31, 2025 to $40.0 million as of June 30, 2026.

In contrast, for the six months ended June 30, 2025, the fair value of the warrant liabilities decreased by $22.4 million, primarily due to a decline in the Company's stock price. The warrant liability decreased from $44.9 million as of December 31, 2024 to $22.5 million as of June 30, 2025.

LIQUIDITY AND CAPITAL RESOURCES

Sources of Liquidity

We do not have any approved products for commercial sale and have never generated revenue from product sales. We have incurred significant net losses and negative cash flows from operations since our inception and expect to continue to incur significant operating losses and negative cash flows from operations for the foreseeable future as we advance the clinical development of our product candidates. As of June 30, 2026, we had cash, cash equivalents and short-term investments of $88.8 million, working capital of $81.3 million and an accumulated deficit of $471.9 million. To date, we have financed our operations primarily through the sale of preferred stock, common stock and warrants.

Our current operating plan, including the planned initiation of a Phase 3 clinical trial in kidney transplantation and continued advancement of our islet cell transplantation program, will require substantial additional capital. We intend to seek additional capital through public or private equity or debt financings, including through our at-the-market equity offering program, or other securities issuances, strategic collaborations, licensing arrangements, credit or loan facilities and other available sources. Our ability to obtain additional financing is dependent on a number of factors, including, but not limited to, market conditions, investor demand for our common stock or other securities, the progress of our development programs and other business risks and uncertainties. There can be no assurance that additional financing will be available when needed or on terms acceptable to us. If we raise capital through the issuance of equity or convertible debt securities, existing stockholders may experience dilution, incur significant financing costs and the new securities may have rights, preferences and privileges senior to those of existing stockholders. If we incur additional indebtedness, it may become subject to additional debt service obligations and operating restrictions.

Based on our current operating plan, we do not currently have sufficient cash, cash equivalents, short-term investments and other available resources to fund our operations for at least twelve months from the date of issuance of the unaudited condensed consolidated financial statements included in this Quarterly Report on Form 10-Q. Accordingly, management has concluded that substantial doubt exists about our ability to continue as a going concern. Although management intends to obtain additional financing through the sources described above, these plans are subject to market conditions and other factors outside our control. Accordingly, management has concluded that its plans do not alleviate the substantial doubt about our ability to continue as a going concern. The accompanying unaudited condensed consolidated financial statements have been prepared on a going concern basis, which contemplates the realization of assets and the satisfaction of liabilities in the normal course of business, and do not include any adjustments that might result from the outcome of this uncertainty.

Material Cash Requirements

Our primary use of cash is to fund operating expenses, which consist of clinical research and development expenses, manufacturing expenses, legal and compliance expenses, compensation and related expenses, and general overhead costs. Cash used to fund operating expenses is impacted by the timing of when we pay or prepay these expenses. As of June 30, 2026, there have been no changes in our material cash requirements from known contractual and other obligations, including commitments for capital expenditures, as disclosed under "Liquidity and Capital Resources-Material Cash Requirements" in Item 7, Management's Discussion and Analysis of Financial Condition and Results of Operations in the 2025 Form 10-K.

We expect our expenses to increase in connection with our ongoing activities, particularly as we expand our clinical program with tegoprubart and continue the research and development of, and seek marketing approval for, our product candidates. In addition, if we obtain marketing approval for any of our product candidates, we expect to incur significant commercialization expenses related to product sales, marketing, manufacturing and distribution.

We will continue to require additional financing in order to advance our drug product through clinical development, to manufacture, obtain regulatory approval for and to commercialize our product candidates, to develop, acquire or in-license other potential product candidates, and to fund operations for the foreseeable future. Therefore, we will seek to raise additional capital through equity offerings, debt financings or other capital sources, including potential collaborations, licenses and other similar arrangements. The ability to raise substantial additional capital will depend on many factors, including:

Conditions in the financial and credit markets may also limit the availability of funding or increase the cost of funding. As a result of any of the foregoing factors, adequate additional funding may not be available to us on acceptable terms on a timely basis, or at all. The severity and duration of any such impacts cannot be predicted. Any such failure to raise capital as and when needed could have a negative impact on our financial condition and on our ability to pursue our business plans and strategies or cause us to delay our clinical development plans, research and development programs or commercialization efforts, out-license intellectual property rights to our product candidates or sell unsecured assets, or a combination of the above. Any of these actions could materially harm our business. The issuance of shares of common stock in our prior private placements and underwritten offerings diluted the ownership interests of our existing stockholders, and to the extent that we raise additional capital through the sale of additional equity, including through our "at-the-market" equity offering program, or convertible debt securities in the future, our stockholders' ownership interests may be further diluted, and the terms of these securities may also include liquidation or other preferences that adversely affect our stockholders' rights. Debt financing, if available, would result in fixed payment obligations and may involve agreements that include restrictive covenants that limit our ability to take specific actions, such as incurring additional debt, making capital expenditures or declaring dividends, that could adversely impact our ability to conduct our business. If we raise funds through collaborations, licenses and other similar arrangements with third parties, we may have to relinquish valuable rights to our technologies, future revenue streams, research programs or product candidates or to grant licenses on terms that may not be favorable to us. Please see Part II, Item 1A. "Risk Factors" in this Quarterly Report on Form 10-Q for additional risks associated with our substantial capital requirements and the challenges we may face in raising capital.

Cash Flows

The following table provides a summary of our net cash flow activity for the six months ended June 30, 2026 and 2025 (in thousands):

Operating Activities

For the six months ended June 30, 2026, operating activities used $45.3 million in cash. This net use of cash reflects our net loss of $70.7 million, adjusted for non-cash items of $33.4 million, consisting primarily of a $28.6 million change in the fair value of warrant liabilities and $5.4 million of stock-based compensation expense, partially offset by $0.8 million related to the accretion of investment discounts. Changes in operating assets and liabilities resulted in an $8.0 million use of cash, primarily driven by a decrease in accrued expenses of $6.0 million related to close-out activities for the Phase 2 BESTOW trial and an increase in prepaid expenses and other assets of $1.8 million related to Phase 3 kidney transplantation trial activities.

For the six months ended June 30, 2025, operating activities used $33.8 million in cash. This net use of cash reflects our net loss of $17.7 million, adjusted for non-cash items of $17.8 million, consisting primarily of a $22.4 million change in the fair value of warrant liabilities and $1.1 million of accretion of investment discounts, partially offset by $5.6 million of stock-based compensation expense. Changes in operating assets and liabilities provided $1.7 million of cash, primarily driven by an increase in accrued expenses.

Investing Activities

Net cash provided by investing activities for the six months ended June 30, 2026 was $29.2 million, consisting of $88.6 million from maturities of available-for-sale short-term investments, partially offset by $59.4 million in purchases of available-for-sale short-term investments.

Net cash provided by investing activities for the six months ended June 30, 2025 was $18.9 million, consisting of $78.1 million from maturities of available-for-sale short-term investments, partially offset by $59.3 million in purchases of available-for-sale short-term investments.

Financing Activities

Net cash provided by financing activities for the six months ended June 30, 2026 consisted of $0.1 million from the exercise of stock options.

Net cash provided by financing activities for the six months ended June 30, 2025 consisted of $0.1 million from the exercise of stock options.