Pharma BD Deal Intelligence
BMS paid $4.8B for Mirati to acquire adagrasib (Krazati), a KRAS G12C inhibitor competing with Amgen's Lumakras in NSCLC. A bet on second-mover advantage—that Mirati's molecule could differentiate on combination potential despite Amgen's first-to-market position.
BMS acquired Mirati Therapeutics for $4.8B for targeted cancer therapies.
FDA granted accelerated approval on June 21, 2024 to adagrasib (KRAZATI) plus cetuximab for adults with KRAS G12C-mutated locally advanced or metastatic…
BMS completes acquisition of Mirati for up to $5.8 billion including contingent value rights, bolstering its oncology pipeline with the KRAS G12C inhibitor…
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BMS acquired Mirati Therapeutics for $4.8B for targeted cancer therapies.
MRTX1719 (Bristol-Myers Squibb/Mirati) is an MTA-cooperative PRMT5 inhibitor in Phase 1/2 targeting MTAP-deleted solid tumors (~10-15% of all cancers, highest in glioblastoma, pancreatic, mesothelioma, and cholangiocarcinoma). No PRMT5 inhibitor is FDA-approved. MTA-cooperative PRMT5 inhibitors (direct MOA rivals with best specificity): AMG 193 (Amgen, Phase 1/2 advanced MTAP-null solid tumors, including NSCLC cohort with registrational intent), TNG908 and TNG462 (Tango Therapeutics, Phase 1/2 with TNG462 showing 20% ORR in pancreatic adenocarcinoma at AACR 2024). First-generation non-selective PRMT5 inhibitors (lower-specificity class): GSK3326595 (EPZ015938, GlaxoSmithKline, discontinued in solid tumors), JNJ-64619178 onametostat (Johnson & Johnson, Phase 1 NSCLC/lymphoma), and PRT543/PRT811 (Prelude Therapeutics, Phase 1). Adjacent synthetic-lethal MTAP strategies: MAT2A inhibitor AG-270 (IDRX/Ideaya/GSK IDE397, Phase 1/2) and methylthioadenosine phosphorylase pathway targeting are complementary threats. Standard-of-care competitors vary by tumor: temozolomide (Temodar) in GBM, gemcitabine/nab-paclitaxel in PDAC, and platinum doublets in mesothelioma. Commercial framing: MRTX1719 competes head-to-head with AMG 193 and Tango's TNG462 for first-to-market MTA-cooperative PRMT5 approval; biomarker-enriched pan-tumor indication is the plausible path given MTAP deletion's tissue-agnostic prevalence.
Adagrasib (Krazati) in KRAS G12C-mutant metastatic colorectal cancer won FDA accelerated approval in June 2024 in combination with cetuximab, based on KRYSTAL-1 ORR of 34%. The competitive set groups cleanly by MOA. KRAS G12C inhibitors (direct class rivals): sotorasib (Lumakras, Amgen) received FDA accelerated approval in January 2025 for KRAS G12C-mutant CRC in combination with panitumumab, supported by CodeBreaK 300 data; divarasib (GDC-6036, Genentech) and garsorasib (D-1553, InventisBio) are in Phase 1b/2. Anti-EGFR monoclonals (combination backbone and share competitor in RAS-wildtype CRC, used off-label contextually): cetuximab (Erbitux, Lilly) and panitumumab (Vectibix, Amgen) drive branded anti-EGFR revenue. Historical standard-of-care chemo backbones still dominate later-line KRAS G12C CRC share: regorafenib (Stivarga, Bayer), trifluridine/tipiracil (Lonsurf, Taiho) with or without bevacizumab (Avastin, Roche), and fruquintinib (Fruzaqla, Takeda) are FDA-approved refractory options unaffected by KRAS status. Commercial implication: adagrasib and sotorasib are effectively duopoly competitors in the ~3-4% G12C-mutant mCRC slice, with differentiation driven by combo partner label, ORR durability, and payer positioning versus Stivarga/Lonsurf/Fruzaqla regimens.
MRTX1133 (Bristol-Myers Squibb/Mirati) is a KRAS G12D-selective non-covalent inhibitor in Phase 1/2, addressing the largest RAS mutant subpopulation (~35% of PDAC, ~13% of CRC, smaller NSCLC fractions). No KRAS G12D-specific agent is FDA-approved. Direct MOA competitors (KRAS G12D selective): ASP3082 (Astellas, pan-KRAS-G12D degrader, Phase 1), HRS-4642 (Jiangsu Hengrui, Phase 1), and INCB161734 (Incyte, Phase 1) are the near-peer pipeline. Pan-KRAS inhibitors (functional substitutes targeting multiple RAS alleles including G12D): RMC-6236 daraxonrasib (Revolution Medicines, Phase 3 RASolute 302 in PDAC), RMC-9805 (Revolution Medicines, KRAS G12D-selective Phase 1), and BI 1823911 (Boehringer Ingelheim, G12C covalent, Phase 1) represent the principal cross-class threat. Upstream RAS-pathway modulators: SOS1 inhibitor MRTX0902 (BMS/Mirati, Phase 2) and SHP2 inhibitors RMC-4630 (Revolution Medicines) and TNO155 (Novartis) are combination backbones. Standard-of-care context (current share holders in G12D-enriched tumors): FOLFIRINOX and gemcitabine/nab-paclitaxel (Abraxane) in PDAC; FOLFOX/FOLFIRI plus bevacizumab (Avastin, Roche) in CRC. Commercial framing: MRTX1133's value depends on beating daraxonrasib's pan-RAS approach on selectivity and tolerability; Revolution Medicines' Phase 3 read-out is the defining competitive event for the G12D segment.
MRTX0902 (Bristol-Myers Squibb/Mirati) is a SOS1 inhibitor in Phase 1/2 as a combination backbone to block KRAS reactivation and adaptive resistance in RAS-driven tumors. No SOS1 inhibitor is FDA-approved. Direct MOA competitors (SOS1 inhibitors): BI 1701963 (Boehringer Ingelheim, Phase 1 combinations with trametinib and adagrasib), BI 3706674 (Boehringer Ingelheim, KRAS G12C-specific SOS1 in preclinical/Phase 1), and RMC-0331 (Revolution Medicines preclinical SOS1) form the near-peer pipeline. Adjacent RAS-pathway combination backbones (functional substitutes): SHP2 inhibitors TNO155 (Novartis, Phase 1/2), RMC-4630 (Revolution Medicines), and JAB-3312 (Jacobio) compete for the same combination-partner slot with KRAS G12C/G12D inhibitors. MEK inhibitors (legacy RAS-pathway combos): trametinib (Mekinist, Novartis), cobimetinib (Cotellic, Roche), and binimetinib (Mektovi, Pfizer) are FDA-approved in BRAF-mutant melanoma/NSCLC and used experimentally in KRAS combinations. Pan-RAS(ON) inhibitors: daraxonrasib (RMC-6236, Revolution Medicines, Phase 3) is the principal strategic threat, potentially obviating the need for SOS1 combinations if monotherapy activity is durable. Commercial framing: MRTX0902 is a platform-enabler rather than a standalone franchise; value accrues through adagrasib combination labels and will be pressured if pan-RAS monotherapy wins the resistance battle.
Adagrasib (Krazati) in KRAS G12C-mutant pancreatic ductal adenocarcinoma is investigational, supported by KRYSTAL-1 Phase 2 data showing 33% ORR in previously treated PDAC. The KRAS G12C mutation is present in only ~1-2% of PDAC (versus ~90% G12D/G12V), which constrains the addressable population. KRAS G12C inhibitors (direct MOA competitors): sotorasib (Lumakras, Amgen) reported 21% ORR in CodeBreaK 100 PDAC cohort per NEJM and is the only cross-tumor competitor with label traction; divarasib (GDC-6036, Genentech) and garsorasib (D-1553, InventisBio) are in Phase 1b/2 basket trials including PDAC. Standard-of-care chemotherapy backbones (no MOA overlap, direct share competitors): FOLFIRINOX and gemcitabine plus nab-paclitaxel (Abraxane, Bristol-Myers Squibb) dominate 1L PDAC; liposomal irinotecan (Onivyde, Ipsen) plus 5-FU/leucorvorin holds 2L approval, and the NALIRIFOX regimen was FDA-approved in February 2024. Broader RAS-targeting pipeline with cross-indication relevance: pan-KRAS inhibitor RMC-6236 (daraxonrasib, Revolution Medicines) is in Phase 3 RASolute 302 for previously treated PDAC. Commercial framing: adagrasib's PDAC opportunity is niche biomarker-defined; competitive pressure will come less from direct G12C rivals than from pan-KRAS agents like daraxonrasib and from standard chemo regimens.
Adagrasib (Krazati) is FDA-approved (December 2022 accelerated, June 2024 full approval pending confirmatory data) for previously treated KRAS G12C-mutant NSCLC, entering a small-molecule targeted class dominated by a direct duopoly. KRAS G12C inhibitors (direct MOA competitors): sotorasib (Lumakras, Amgen) received first-in-class FDA approval in May 2021 and holds the leading share in post-platinum G12C NSCLC; divarasib (GDC-6036, Roche/Genentech) posted 53% ORR in Phase 1b and is in registrational development; garsorasib (D-1553, InventisBio/Jiangsu Hengrui), olomorasib (LY3537982, Eli Lilly), and opnurasib (JDQ443, Novartis) are Phase 1/2. Broader competitive context in 2L+ NSCLC without driver-stratification: platinum-doublet chemotherapy plus pembrolizumab (Keytruda, Merck) or nivolumab (Opdivo, BMS) remain 1L standard, and docetaxel plus ramucirumab (Cyramza, Lilly) is a guideline 2L option. Emerging pan-RAS/SOS1 pathway modulators such as BMS' own MRTX0902 (SOS1) and revumenib-adjacent combinations represent next-wave threats. Commercial framing: Krazati and Lumakras together cover roughly 13% of NSCLC adenocarcinomas (KRAS G12C prevalence). Lumakras reported $280M global net sales in FY2023 per Amgen 10-K, setting the ceiling adagrasib must displace through CNS-penetrant data, combination strategies, and payer access.
BMS completed $4.8B acquisition of Mirati Therapeutics ($58/share plus CVR), gaining Krazati (adagrasib) KRAS G12C inhibitor and next-gen KRAS pipeline.
FDA granted accelerated approval for Krazati plus cetuximab in KRAS G12C-mutated metastatic colorectal cancer, expanding beyond initial NSCLC indication.
BMS removed MRTX0902 from pipeline while retaining MRTX1719 (Phase 1 for MTAP-deleted solid tumors), narrowing the acquired Mirati pipeline.
Krazati gained a second FDA indication in CRC but faces competition from Amgen's Lumakras. One pipeline asset dropped. Commercial trajectory uncertain for $4.8B.
| Deal | Year | Value | Outcome |
|---|---|---|---|
| Bristol-Myers Squibb Company / Mirati Therapeutics (this deal) | 2023 | $4.8B | 66 |
| Bristol-Myers Squibb Company / Medarex Inc. | 2009 | $2.4B | 92 |
| Bristol-Myers Squibb Company / Celgene Corporation | 2019 | $74.0B | 77 |
| Bristol-Myers Squibb Company / MyoKardia Inc. | 2020 | $13.1B | 76 |
| Bristol-Myers Squibb Company / Karuna Therapeutics | 2023 | $14.0B | 76 |
| Bristol-Myers Squibb Company / Ono Pharmaceutical Co., Ltd. | 2011 | — | 76 |
| Bristol-Myers Squibb Company / SystImmune Inc. | 2023 | $8.4B | 71 |
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