CTX-471 / CD137 agonist

CTX-471 is a fully human monoclonal antibody that binds and activates a novel epitope of the co-stimulatory receptor CD137, also known as 4-1BB, a member of the tumor necrosis factor receptor superfamily.

Preclinical data presented at the 2018 Society for Immunotherapy of Cancer Annual Meeting suggest that CTX has the potential to become a best-in-class CD137 agonist displaying curative monotherapy efficacy against multiple syngeneic tumor models and generation of long-term functional immunological memory. Most notably, CTX-471 is able to induce the complete eradication of large, established tumors where other preclinical CD137 antibodies and antibodies against PD-1, PDL, CTLA, and OX40 have minimal effect. CTX-471 profoundly reprograms the tumor microenvironment, increasing CD8+ T cell infiltration and penetration while reducing T-cell exhaustion. In contrast to other clinical and preclinical CD137 antibodies, CTX-471 shows no evidence of hepatic inflammation and toxicity in both mice and non-human primates, supporting a wide therapeutic window.

We are now enrolling patients in a Phase 1 clinical trial of CTX-471. Visit clinicaltrials.gov for more information.

CTX-471 Combination

CTX-471 is a fully human monoclonal antibody that binds and activates a novel epitope of the co-stimulatory receptor CD137, also known as 4-1BB, a member of the tumor necrosis factor receptor superfamily.

In preclinical combination sudies, CTX-471 significantly enhances the efficacy of other IO agents including tumor targeting antibodies cetuximab (Erbitux) and trastuzumab (Herceptin), checkpoint inhibitors against PD-1 and PD-L1, and small molecule inhibitors of CXCR2.

CTX-8371 / PD-1 x PD-L1

CTX-8371 is a common light chain-based, bispecific antibody targeting the checkpoint receptor PD-1 and its ligand PD-L1. Discovered via an unbiased screen of bispecifics targeting checkpoint combinations using our StitchMabsTM platform, CTX-8371 enhances T cell activation and tumor cell killing in vitro and in vivo with significantly increased potency compared to Keytruda and other approved PD-1/PDL-1 therapies. Mechanistic studies suggest that the enhanced efficacy is due to a unique ability of this bispecific to drive PD-1 downregulation and degradation in T cells.