IDEAYA Biosciences and Genentech will run a clinical study pairing IDEAYA's MTA-cooperative PRMT5 inhibitor IDE892 with GDC-7035, also known as RG6620, Genentech's Phase 1 KRAS G12D inhibitor, in pancreatic ductal adenocarcinoma carrying both an MTAP deletion and a KRAS G12D mutation. Genentech sponsors the trial and IDEAYA supplies its drug, with no license or transfer of rights in either direction. IDEAYA says patients with both alterations have no approved targeted option today.
- Announced: August 19, 2026, from South San Francisco.
- Combination: IDE892, an MTA-cooperative PRMT5 inhibitor, plus Genentech's GDC-7035 (RG6620).
- Who does what: Genentech sponsors the trial, IDEAYA supplies IDE892, and a joint governance body oversees the clinical supply collaboration.
- Rights: each party keeps all commercial rights to its own compound, as monotherapy and in combination.
- Population: MTAP deletion and KRAS G12D are estimated to co-occur in up to approximately 15 percent of PDAC patients.
- Selectivity claim: roughly 1,400-fold cooperative binding to MTA-PRMT5 over SAM-PRMT5, per IDEAYA.
Who Sponsors and Who Supplies
The two companies described a clinical supply collaboration in an announcement issued August 19. Genentech will sponsor the study, IDEAYA will hand over IDE892, and joint governance will oversee the work, with no upfront payment, milestone or royalty named in the release.
This extends an existing thread with Roche. IDEAYA said it plans to open a Phase 1 combination cohort with Roche's RG6505 in MTAP-deleted, RAS-mutant PDAC in the second half of 2026. Separately, IDE892 is in Phase 1 dose escalation and expansion in MTAP-deleted solid tumors, and a combination cohort with IDEAYA's own MAT2A inhibitor IDE397 has opened in non-small cell lung cancer and other solid tumors.
A Second KRAS Pairing With Roche
"We are excited to expand our clinical collaboration with Roche to evaluate a second KRAS combination with potential best-in-class MTA-cooperative PRMT5 inhibitor IDE892 for pancreatic cancer patients, where there remains a high unmet medical need," said Yujiro S. Hata, president and chief executive officer of IDEAYA Biosciences. He listed IDE397, pan-RAS inhibitors, KRAS G12D inhibitors and the company's lead CDKN2A compound as the combination strategies being built around IDE892.
Combining a PRMT5 inhibitor with a KRAS G12D mutant-specific drug may drive deeper and more durable responses in the dual-altered group, the companies said. That framing belongs to the sponsors, and no clinical data for the pairing has been released.
IDEAYA Puts Cooperative Binding at 1,400-Fold
IDEAYA puts IDE892's cooperative binding to MTA-PRMT5 at approximately 1,400-fold over SAM-PRMT5 binding, and reports that the molecule does not penetrate the brain, both offered by the company as evidence of a wider therapeutic window. The release also carries the pharmacology that matters when two investigational agents share a dosing schedule. IDE892 showed a CYP3A4 IC50 greater than 45 micromolar and no time-dependent inhibition of any of the seven major cytochrome P450 enzymes tested, CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, in full kinetic inactivation assays. Those are company-reported preclinical figures.
Enrollment Turns on Two Findings at Once
Nothing in the announcement says how MTAP deletion or KRAS G12D status will be established for eligibility, whether a central laboratory will do the screening, or when the trial opens. IDEAYA's own risk disclosure lists "the ability to successfully identify and enroll patients with the relevant molecular alterations in clinical trials" among the factors that could change the outcome, and points to the annual report on Form 10-K it filed with the Securities and Exchange Commission on February 17, 2026.
Why This Matters to the APO|APE Reader
Genentech carrying the sponsor's obligations puts protocol design and the prescreening burden inside Roche's trial machinery, while IDEAYA's exposure stays at the level of drug supply. The consequence for laboratories arrives further out. Any combination that advances would need an agreed way to call MTAP loss alongside a specific KRAS codon change, and no companion diagnostic has been named for either agent. The second-half 2026 start IDEAYA has flagged for the separate RG6505 cohort gives a rough sense of when a second Roche pairing joins the same screening queue for the same small pancreatic population.
