GIM-531 Advanced Drug Monograph

Name: GIM-531 Name (English): GIM-531

Developer: Georgiamune Inc.

Status: Currently in Phase 1/2 clinical trials.

Mechanism of Action: Selective T regulatory cell (Treg) inhibitor. It is designed to inhibit the induction and function of Tregs, which are suppressor immune cells that can impede the body's anti-tumor responses. By inhibiting Tregs, GIM-531 aims to reprogram the tumor microenvironment to allow the immune system to eliminate cancer cells.

Route of Administration: Oral.

Indication: Advanced solid tumors, including metastatic cutaneous melanoma, that have progressed on or are intolerant of standard therapies, or cancers not adequately addressed by existing immunotherapies like anti-PD-1 antibodies. Specific cohorts in the clinical trial include single-agent treatment in tumors where Tregs play a significant role and combination therapy with anti-PD-1 in anti-PD-1 failure advanced melanoma.

Clinical Trials: A Phase 1/2 open-label, multi-center study (GIM531-CT01) is ongoing to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamic effects, and preliminary efficacy of GIM-531 as a single agent and in combination with an anti-PD-1 antibody in patients with advanced solid tumors. The Phase 1 portion focuses on dose escalation, while the Phase 2 portion will assess anti-tumor activity in specific tumor types and in combination with anti-PD-1 therapy.

Rationale: GIM-531 represents a novel approach to cancer immunotherapy by targeting Tregs, which are often enriched in the tumor microenvironment and contribute to immune suppression. Inhibiting Tregs may enhance the effectiveness of the body's own immune system to fight cancer and potentially overcome resistance to other immunotherapies.

Additional Information: GIM-531 is considered a first-in-class oral immunotherapy. Georgiamune believes it can address a critical unmet need in oncology, particularly for patients with "cold" tumors (unlikely to trigger a strong immune response) and those who have developed resistance to PD-1 inhibitors.