GLUE News & Events

"We continue to make excellent progress advancing multiple programs through the clinic, with all three of our clinical-stage programs approaching Phase 2 trial initiations," said Markus Warmuth, Chief Executive Officer of Monte Rosa Therapeutics. "Building on interim clinical data for our NEK7-directed MGD MRT-8102 demonstrating rapid, deep, and durable reductions in systemic inflammation, we expect to read out the GFORCE-1 study in subjects with elevated cardiovascular disease risk this year, and to initiate three Phase 2 studies, starting in H2 2026, in diseases driven by the NLRP3/IL-1/IL-6 pathway. We also expect our collaborator Novartis to initiate multiple Phase 2 studies of our VAV1-directed MGD MRT-6160 in immune-mediated diseases this year. In addition, our oncology programs are also progressing rapidly, in particular with a Phase 2 study initiation of MRT-2359 in metastatic castration-resistant prostate cancer patients with androgen receptor mutations planned for Q3 2026, following the encouraging Phase 1/2 data we presented at ASCO GU."

Monte Rosa Therapeutics announced the company will present preclinical data highlighting the potential of its highly selective, first-in-class cyclin E1-directed MGD, MRT-55811, to treat CCNE1-amplified solid tumors at the American Association for Cancer Research, AACR, Annual Meeting 2026, being held April 17-22 in San Diego, CA. Summary of Results: MRT-55811 exhibited potent degradation and high selectivity for CCNE1, with no detectable degradation of closely related cyclins or cyclin-dependent kinases, and favorable drug-like properties. MRT-55811 induced deep cyclin E1 degradation and downstream pathway suppression, as well as co-degradation of CDK2 within the cyclin E1/CDK2 holoenzyme complex in CCNE1-amplified cell lines. MRT-55811 demonstrated superior selectivity compared with clinical-stage CDK2 inhibitors, which exhibited significant off-target activity, as evidenced by kinome profiling and genetic modeling. In CCNE1-amplified cancer cell lines, MRT-55811 selectively inhibited cellular proliferation, while sparing cell lines without amplification. In vivo, MRT-55811 monotherapy resulted in tumor regression and pathway suppression in multiple CCNE1-amplified models. MRT-55811 downmodulated retinoblastoma protein phosphorylation and E2F-driven gene expression, demonstrating on-target effects in tumors grown in vivo.