Durvalumab combined with neither BA3011 nor BA3021 demonstrated sufficient efficacy to proceed to second stage accrual. No new safety signals were identified. We showed the feasibility of collecting and analyzing tissue in this platform study.

ADCT-601 demonstrates robust AXL expression linked to anti-tumor activity in preclinical models of ACC, establishing a proof of concept for targeting AXL in this rare cancer. These findings support clinical translation of AXL-targeting ADC as a novel biomarker-driven therapy for patients with ACC.

ADCT-601 demonstrates robust AXL expression linked to anti-tumor activity in preclinical models of ACC, establishing a proof-of-concept for targeting AXL in this rare cancer. These findings support clinical translation of AXL-targeting ADC as a novel biomarker-driven therapy for patients in ACC.

EnaV had an acceptable safety profile; however, because the evaluation of antitumor activity did not show clinically meaningful responses, clinical development of EnaV was discontinued.

P2, N=85, Completed, BioAtla, Inc. | Active, not recruiting --> Completed | N=240 --> 85

P1/2, N=245, Completed, BioAtla, Inc. | Active, not recruiting --> Completed | Trial completion date: Jun 2025 --> Jan 2025

P1/2, N=300, Active, not recruiting, BioAtla, Inc. | Trial completion date: Jan 2025 --> Jun 2025

Furthermore, in nonhuman primates, mecbotamab vedotin demonstrated excellent tolerability at doses of up to 5 mg/kg and maintained linker-payload stability in vivo. These findings indicate that mecbotamab vedotin has the potential to be a robust and less toxic therapeutic agent, offering promise as a treatment for patients with AXL-positive cancers.

P1, N=128, Terminated, ADC Therapeutics S.A. | N=260 --> 128 | Trial completion date: Aug 2027 --> Apr 2025 | Active, not recruiting --> Terminated | Trial primary completion date: Aug 2026 --> Apr 2025; Sponsor decided to halt further development of ADCT-601

Immunotherapeutic strategies for neuroblastoma must address the potential of epigenetic downregulation of antigen density as a mechanism for immune evasion. We identified several RTKs as candidate MES-specific immunotherapeutic target proteins for the elimination of therapy-resistant cells. We hypothesize that the phenomena of immune escape will be less likely when targeting pan-neuroblastoma cell surface proteins such as B7-H3 and L1CAM, and/or dual targeting strategies that consider both the ADRN- and MES-cell states.

P1/2, N=300, Active, not recruiting, BioAtla, Inc. | Recruiting --> Active, not recruiting

P1, N=260, Active, not recruiting, ADC Therapeutics S.A. | Recruiting --> Active, not recruiting