CRVS

Given these uncertainties, you should not place undue reliance on these forward-looking statements.
Any product candidate we or any of our existing or potential future collaborators advance into clinical trials, including soquelitinib, ciforadenant and mupadolimab , may not have favorable results in later clinical trials, if any, or receive regulatory approval. ● Any termination or suspension of, or delays in the commencement or completion of, our planned clinical trials could result in increased costs to us, delay or limit our ability to generate revenue and adversely affect our commercial prospects. ● Our product candidates are subject to extensive regulation, compliance with which is costly and time consuming, and such regulation may cause unanticipated delays or prevent the receipt of the required approvals to commercialize our product candidates. ● We are conducting and plan to conduct clinical trials for soquelitinib , ciforadenant and mupadolimab, and we and Angel Pharmaceuticals may in the future, conduct additional clinical trials of product candidates at sites outside the United States, and the FDA may not accept data from trials conducted in foreign locations. ● If we encounter difficulties enrolling subjects in our clinical trials, our clinical development activities could be delayed or otherwise adversely affected. iv ● The occurrence of serious complications or side effects in connection with use of our product candidates, either in clinical trials or post-approval, could lead to discontinuation of our clinical development programs, refusal of regulatory authorities to approve our product candidates or, post-approval, revocation of marketing authorizations or refusal to approve new indications, which could severely harm our business, prospects, results of operations and financial condition. ● We may not be successful in our efforts to identify or discover additional product candidates. ● We rely, and expect to continue to rely, on third parties to conduct our clinical trials.
We believe our proprietary product candidates have broad potential to address immune mediated diseases, inflammatory diseases and cancers.
Based on the proposed mechanism of action, we believe soquelitinib has the potential to be utilized to inhibit the production of a number of inflammatory cytokines involved in diseases such as atopic dermatitis, hidradenitis suppurativa, asthma, psoriasis and fibrotic diseases.
In preclinical studies, Soquelitinib has affected T cell differentiation leading to enhanced function of T cells involved in tumor cell eradication.
Soquelitinib entered both a registrational, Phase 3 clinical trial for relapsed T cell lymphomas and a recently initiated randomized, placebo-controlled Phase 2 trial in patients with atopic dermatitis.
Product Candidate Pipeline Our product candidate pipeline and anticipated milestones include the following: (1) The Company did not conduct Phase 1 studies for these specific indications, but is planning to initiate Phase 2 studies for these indications based on the Phase 1 Atopic Dermatitis study.
Mice with genetic knock-out of ITK also demonstrate a reduction in Th2 and Th17 cells, which produce the cytokines that are often responsible for autoimmunity and allergy such as interleukin (Il) Il-4, Il-5, Il-13, Il-17 and many others.
Selective inhibition of ITK can block the production and function of Th2 and Th17 helper T cells, potentially leading to a biasing toward the differentiation of naïve T cells into Th1 helper T cells.
Soquelitinib is currently being studied both in cancer and in immune mediated diseases.
The study is now complete, however, some of the patients remain on therapy and are continuing to receive follow-up monitoring.
The trial enrolled 75 patients (27 in the dose escalation portion and 48 in dose expansion portion) with various T cell lymphomas, including peripheral T cell lymphoma (“PTCL”), T follicular helper cell lymphoma, natural killer cell T cell lymphoma, cutaneous T cell lymphoma, anaplastic large cell lymphoma and adult T cell lymphoma/leukemia.
The median number of prior therapies was three (range 1-18), with only 31% achieving an objective response to their most recent prior therapy.
In the dose escalation portion, patients received a twice-daily dose of soquelitinib of 100 mg, 200 mg, 400 mg or 600 mg, and the 200 mg twice-daily dose (“200 mg BID”) was selected for the dose expansion portion based on biomarker studies indicating that doses of 200 mg or higher achieved complete occupancy of the ITK target with the drug.
Final data from the Phase 1/1b clinical trial were presented at the American Society of Hematology Annual Meeting (“ASH”) in December 2025.
Key highlights from the data supporting the ongoing registration Phase 3 trial in relapsed/refractory PTCL include: ● No dose limiting toxicities or significant adverse events were observed in any patients in all dose cohorts up to 600 mg twice-daily, including no myelosuppression or immunosuppression; ● Objective and durable tumor responses were seen in the 200 mg twice-daily cohort (N=36) with 6 patients experiencing complete responses; ● In the 200 mg twice-daily cohort, it was determined that patients with between ≥1 and ≤3 prior therapies and an adequate peripheral blood lymphocyte count (N=24) were most likely to be responders to therapy.
In this patient population: o Objective responses were seen in 9 of 24 patients including 6 complete responses and 3 partial responses; o Median progression free survival (“PFS”) was 6.2 months, including an 18-month PFS of 30%; and o Median overall survival (“OS”) was 28.1 months, including a 24-month OS of 67% Key highlights from the data supporting soquelitinib’s proposed mechanism of action (Th1 skewing and blocking Th2 and Th17 differentiation) and development in immune and inflammatory diseases include: ● In vitro studies demonstrated that at appropriate doses, soquelitinib produced Th1 skewing, which is an immunologic property resulting from the blockade of Th2 differentiation and a shift to Th1; ● Biomarker studies evaluating blood samples and tumor biopsies showed an increase in Th1 in blood and tumor samples and a reduction in serum IL-5, consistent with inhibiting Th2 and Th17 cells; and ● For six patients, paired tumor biopsies were compared at baseline and day 8 and showed an increase in intratumor Th1 cells with treatment analyzed using RNA sequencing.
The clinical trial was planned to enroll 64 patients into one of four dosing cohorts in a 3:1 ratio (12 active and 4 placebo) to receive either soquelitinib or placebo.
The cohorts were designed to sequentially enroll and to examine 100 mg oral twice per day, 200 mg oral once per day, 200 mg oral twice per day and 400 mg oral once per day.
Patients would be treated for 28 days and are then followed for an additional 30 days with no therapy.
The primary endpoints included safety and tolerability, and efficacy, measured by improvement in Eczema Area and Severity Index (“EASI”) score, Investigator Global Assessment (“IGA”), reduction in itch and various cytokine biomarkers.
As of May 6, 2025, enrollment into cohorts 1, 2 and 3 had been completed and we reported interim data for a total of 48 patients.
These data covered 32 patients receiving soquelitinib and 12 receiving placebo with 28-day follow-up, and four additional patients receiving soquelitinib with 15-day follow-up from cohort 3.
These four patients had not yet completed the 28-day treatment course.
The percent reduction in mean EASI scores at 28 days for the combined cohort 1 and 2 group was 54.6% for patients receiving soquelitinib and 30.6% for patients receiving placebo.
In cohort 3, the 200 mg BID cohort, the percent reduction in mean EASI score at 28 days was 71.1% for patients receiving soquelitinib and 42.1% for patients receiving placebo.
On January 20, 2026, we announced positive results from cohort 4 of our randomized, blinded, placebo-controlled Phase 1 clinical trial evaluating soquelitinib in patients with moderate to severe atopic dermatitis.
Based on the encouraging results from cohorts 1-3, cohort 4 was prospectively redesigned to support and potentially extend the clinical results obtained in the initial cohorts.
Cohort 4 was expanded to enroll 24 patients randomized 1:1 to receive soquelitinib 200 mg BID (the same dose as cohort 3) or placebo and the treatment period was extended to 56 days from the 28-day treatment period used for cohorts 1-3.
The cohort 4 data demonstrated favorable safety and efficacy results consistent with results from cohorts 1-3, including a deepening of responses in cohort 4 over the 8-week treatment period compared to the 4-week treatment period.
The results also showed clinical activity in patients who had received prior systemic therapies, including patients resistant to therapies like dupilumab and JAK inhibitors.
We believe the data to-date also support the novel proposed mechanism of action with ITK inhibition, which is designed to act upstream and regulate multiple T cell functional pathways.
We believe the immune rebalancing shown thus far by soquelitinib shows its potential in a wide range of inflammatory and immune diseases.
Based on these positive results, we plan to initiate a Phase 2 trial evaluating soquelitinib in patients with moderate to severe atopic dermatitis that have failed at least one prior topical or systemic therapy in the first quarter of 2026.
As of January 15, 2026, enrollment in cohort 4 was completed and all soquelitinib treated patients (n=12) had completed the 56-day treatment course.
Of the 12 enrolled placebo patients, 10 were evaluable at day 56, as two patients were non-compliant and missed the day 56 visit; these two patients completed additional follow up at later time points.
Patients in cohort 4 had similar baseline characteristics compared to patients in cohort 3, with patients in these cohorts having more advanced disease with a higher mean baseline EASI score compared to patients in cohorts 1 and 2.
The mean baseline EASI in cohort 4 was 25.7 for the patients treated with soquelitinib and 21.9 for patients that received placebo.
Across all four cohorts (n=72), 35% of patients had received prior systemic therapies (n=25), including 50% of patients (n=12) in cohort 4.
Overall, all four cohorts showed meaningful responses in the soquelitinib treatment groups compared to placebo for clinically significant endpoints of EASI 75 and IGA 0 or 1.

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Gone since FY2024

Given these uncertainties, you should not place ii undue reliance on these forward-looking statements.
Any product candidate we or any of our existing or potential future collaborators advance into clinical trials, including soquelitinib, ciforadenant and mupadolimab , may not have favorable results in later clinical trials, if any, or receive regulatory approval. ● Any termination or suspension of, or delays in the commencement or completion of, our planned clinical trials could result in increased costs to us, delay or limit our ability to generate revenue and adversely affect our commercial prospects. ● Our product candidates are subject to extensive regulation, compliance with which is costly and time consuming, and such regulation may cause unanticipated delays or prevent the receipt of the required approvals to commercialize our product candidates. ● We are conducting and plan to conduct clinical trials for soquelitinib , ciforadenant and mupadolimab, and we and Angel Pharmaceuticals may in the future, conduct additional clinical trials of product candidates at sites outside the United States, and the FDA may not accept data from trials conducted in foreign locations. ● If we encounter difficulties enrolling subjects in our clinical trials, our clinical development activities could be delayed or otherwise adversely affected. iv ● The occurrence of serious complications or side effects in connection with use of our product candidates, either in clinical trials or post-approval, could lead to discontinuation of our clinical development programs, refusal of regulatory authorities to approve our product candidates or, post-approval, revocation of marketing authorizations or refusal to approve new indications, which could severely harm our business, prospects, operating results and financial condition. ● We may not be successful in our efforts to identify or discover additional product candidates. ● We rely, and expect to continue to rely, on third parties to conduct our clinical trials.
We believe our proprietary product candidates have broad potential to address cancers, immune mediated diseases and inflammatory diseases.
Based on the proposed mechanism of action, we believe soquelitinib has the potential to be utilized to inhibit the production of a number of inflammatory cytokines involved in diseases such as atopic dermatitis, asthma, psoriasis and fibrotic diseases.
In preclinical studies, Soquelitinib has affected T cell differentiation leading to enhanced function of T cells involved in tumor cell killing.
Soquelitinib entered a registrational, Phase 3 clinical trial for relapsed T cell lymphomas and is also being evaluated in a randomized, placebo controlled Phase 1 trial in patients with atopic dermatitis.
Product Pipeline Our product candidate pipeline and anticipated milestones include the following: Soquelitinib (CPI-818), ITK Inhibitor.
Mice with genetic knock-out of ITK also demonstrate a reduction in Th2 cells, which produce the cytokines that are often responsible for autoimmunity and allergy such as interleukin (Il) Il-4, Il-5, Il-13, Il-17 and many others.
Selective inhibition of ITK can block the production and function of Th2 and Th17 helper T cells, potentially leading to a biasing toward the differentiation of naïve T cells into Th1 helper T cells, a process known as Th1 skewing.
Soquelitinib is currently being studied both in cancer and in immune mediated disease.
The study is no longer enrolling new patients, however, some of the patients remain on therapy and are continuing to receive follow-up monitoring.
The study employs an adaptive, expansion cohort design, with an initial phase that evaluated escalating doses (100, 200, 400 or 600 mg taken twice a day) in successive cohorts of patients, followed by a second phase that was designed to evaluate safety and tumor response to the recommended dose of soquelitinib in disease-specific patient cohorts.
The study has enrolled patients from the United States, Australia, China and South Korea with several types of advanced, refractory T cell lymphomas.
No dose limiting toxicities were observed in any of the dose levels.
As of November 27, 2024, and in a safety population of 75 patients, no hematologic, renal or hepatic treatment-related adverse events were observed and the most common grade 3 to 4 adverse event was pruritus, seen in four patients with lymphoma involving skin.
The optimum dose was determined to be 200 mg twice per day based on anti-tumor efficacy and pharmacodynamic studies which revealed full occupancy of the ITK active site by the drug.
This dose was also consistent with dose-response effects seen in preclinical experiments both in vitro and in vivo.
Interim data from the Phase 1/1b clinical trial were presented at the American Society of Hematology Annual Meeting (“ASH”) in December 2023.
At that time, we also announced interim data from the trial as of November 21, 2023 on 21 evaluable patients receiving a dose of 200 mg twice per day (“200 mg BID”) and revealed an objective response rate (“ORR”) of 33.3% with 3 complete responses (“CRs”) and 4 partial responses (“PRs”).
As of July 16, 2024, 25 patients (≤ 3 prior therapies) were enrolled in the trial at the 200 mg BID dose, including 23 evaluable patients.
For the 23 evaluable patients, objective responses (CR plus PR) were seen in nine patients (39%), including six CRs (26%) and three PRs.
The median progression free survival was 6.2 months.
As of November 27, 2024, four of the responding patients remained on therapy; 3 with CRs and one with a PR.
In July 2024, soquelitinib received Fast Track designation for treatment of adult patients with relapsed or refractory peripheral T cell lymphoma after at least 2 lines of systemic therapy.
As reported at the International Conference of Malignant Lymphoma in June 2023, preclinical data suggest that ITK inhibition with soquelitinib has the potential to treat solid and hematological cancers based on its novel proposed mechanism of action.
Tumor immune responses were enhanced by the modulation of T cell differentiation resulting in increased T cell cytolytic capacity, increased migration of T cells into the tumor and reduced T cell exhaustion.
Highlights of the presentation included: ● monotherapy provided statistically significant inhibition of tumor growth in established tumors in the following cancer models: EL4 TCL (T cell lymphoma), A20 B cell lymphoma and CT26 colon cancer. ● In the EL4 TCL model, treatment with soquelitinib led to increased infiltration of normal CD8+ T cells into the tumor.
In addition, these CD8+ T cells had higher expression of perforin, an effector molecule produced by killer T cells that is involved in killing cancer cells. ● In the CT26 colon cancer model, the depletion of normal CD8 cells reduced the activity observed for soquelitinib treatment, suggesting that its potential mechanism of action involves the production of normal CD8+ T cells. ● In the CT26 colon cancer model, treatment with soquelitinib reduced the expression of T cell exhaustion markers.
T cell exhaustion is a phenomenon seen in tumors and chronic infections where prolonged exposure to antigens results in exhausted or ineffective T cell function and inability to eliminate tumors or infections. ● In other murine studies using antigen primed T cells that were repeatedly stimulated, soquelitinib reduced the development of T cell exhaustion and reversed it in already exhausted T cells.
These reinvigorated T cells regained their cancer cell killing capacity.
We believe these findings suggest that the inhibition of ITK by soquelitinib produced changes in the tumor microenvironment that enhanced anti-tumor immunity creating a less favorable environment for tumor growth and provides the rationale for clinical investigation in a monotherapy trial of soquelitinib in solid tumors.
We are planning a Phase 1b/2 clinical trial, in collaboration with the Kidney Cancer Research Consortium, of soquelitinib in solid tumors in patients with renal cell cancer who have failed checkpoint inhibitor therapy.
The clinical trial is planned to enroll 64 patients into one of four dosing cohorts in a 3:1 ratio (12 active and 4 placebo) to receive either soquelitinib or placebo.
The cohorts are sequentially enrolled and will examine 100 mg oral twice per day, 200 mg oral once per day, 200 mg oral twice per day and 400 mg oral once per day.
Patients are treated for 28 days and are then followed for an additional 30 days with no therapy.
The primary endpoints include safety and tolerability, and efficacy, measured by improvement in Eczema Area and Severity Index (“EASI”) score, Investigator Global Assessment (“IGA”), reduction in itch and various cytokine biomarkers.
Corvus and a data monitoring committee will be able to monitor the data from the trial as the trial progresses.
On January 13, 2025, we reported top-line results from 16 patients in Cohort 1 (12 patients in the soquelitinib group receiving 100 mg orally twice per day vs. four receiving placebo) and 10 patients in Cohort 2 (seven patients in the soquelitinib group receiving 200 mg orally once per day vs. three receiving placebo) for which 28 days of treatment had been completed.
For those 19 patients in the soquelitinib group, 26% achieved IGA 0 or 1 and 37% achieved EASI 75; and of the seven in the placebo group, none achieved IGA 0 or 1 or EASI 75.
No significant safety issues were observed and no clinically significant laboratory abnormalities were seen.

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