talabostat (BXCL701)

P1/2, N=98, Completed, BioXcel Therapeutics Inc | Active, not recruiting --> Completed | Phase classification: P1b/2 --> P1/2 | Trial completion date: Dec 2025 --> Dec 2024

P2, N=22, Active, not recruiting, Georgetown University | Recruiting --> Active, not recruiting | N=43 --> 22 | Trial primary completion date: Nov 2026 --> Jan 2026

P2, N=31, Terminated, M.D. Anderson Cancer Center | N=15 --> 31 | Trial completion date: Dec 2025 --> Mar 2025 | Active, not recruiting --> Terminated | Trial primary completion date: Dec 2025 --> Mar 2025; There is no PR/CR observed in the first stage, so study stopped without proceeding to the stage 2 of efficacy stage.

P2, N=15, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Apr 2025 --> Dec 2025 | Trial primary completion date: Apr 2025 --> Dec 2025

In this investigation, PT-100 (also referred to as Talabostat, Val-boroPro, and BXCL701), an orally administered and nonselective dipeptidyl peptidase inhibitor, not only augmented the effectiveness of anti-PD-1 therapy but also significantly improved T immune cell infiltration and reversed the immunosuppressive tumor microenvironment...The results further suggested that PT-100 dramatically reduced the ratio of tumor-associated macrophages. These findings provide a promising combination strategy for immunotherapy in lung cancer.

P2, N=15, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Apr 2024 --> Apr 2025 | Trial primary completion date: Apr 2024 --> Apr 2025

Gemcitabine (GEM) is commonly used as the first-line chemotherapeutic agent for treating pancreatic cancer (PC) patients. The activation of CASP1 by the DPP8/DPP9 inhibitor (Val-boroPro, VbP) increased GEM-induced cell death by inducing pyroptosis. These findings suggest that inhibiting CASP1 to suppress its oncogenic effects or activating it to promote cell pyroptosis both enhance the sensitivity of PC cells to GEM therapy.

Major eligibility criteria include: ≥18 years of age, relapsed or refractory AML or relapsed or refractory MDS with ≥10%.refractory to at least 4 cycles of hypomethylating agent, ECOG performance status ≤2, adequate renal function (CrCl ≥30 mL/min), adequate liver function (total bilirubin ≤1.5 x ULN, ALT and AST ≤3 x ULN), WBC 100 days from allogeneic bone marrow transplant with no active graft versus host disease...There will be a second phase of the study that will evaluate BXCL701 in combination with a hypomethylating agent (decitabine or azacytidine) and venetoclax. The trial is currently open and continuing to enroll.

Additional biomarker analyses are ongoing to build on this finding. It will also be validated in the randomized Phase 2b SCNC trial planned to initiate in 2H 2023.

Talabostat treatment in the co-culture models reverses CAF-induced suppression of T cell proliferation. Conclusions Talabostat reverses stromal-mediated T cell suppression and is a potential therapeutic strategy to elicit a more effective immune response.

P2, N=43, Recruiting, Georgetown University | Not yet recruiting --> Recruiting

P1b/2, N=98, Active, not recruiting, BioXcel Therapeutics Inc | Recruiting --> Active, not recruiting | N=240 --> 98