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#小分子/降解剂

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Oct 15Thu
  1. ema.europa.eu90

    EMA recommends authorisation of Rasonque for metastatic pancreatic cancer

    EMA's CHMP has recommended EU marketing authorisation for Revolution Medicines' Rasonque (daraxonrasib), an oral RAS inhibitor for adults with metastatic pancreatic adenocarcinoma previously treated at least once. In a 500-patient phase 3 study, median overall survival was 12.4 months versus 6.7 with chemotherapy, and median progression-free survival 7.2 versus 3.6 months. The European Commission will now fast-track its decision, with pricing left to Member States.

    Why it matters: CHMP backing via a phased review under 150 days sets precedent for faster EU assessments of priority cancer medicines.

  2. doi.org48

    Open-label extension study of leniolisib in activated PI3Kδ syndrome: Long-term efficacy and safety

    Long-term leniolisib was generally well tolerated in 37 patients with activated phosphoinositide 3-kinase delta syndrome treated for a median of 4.3 years. Annual infection rates (P = 0.0005), respiratory infection rates (P = 0.0017) and immunoglobulin replacement therapy use (P = 0.0095) all declined per year of treatment, with clinically meaningful gains in 36-Item Short Form Survey general health scores. This extends the efficacy and safety evidence for leniolisib in APDS well beyond the pivotal trials.

  3. biorxiv.org40

    A Multi-Kinase Inhibitor Screen Identifies mTOR Signaling as a Vulnerability in Advanced Prostate Cancer.

    Loss of the receptor tyrosine kinase AXL is linked to treatment resistance, aggressive phenotypes, and shorter overall survival in prostate cancer. Screening isogenic CRISPR-generated AXL-knockout cells against 1,814 kinase inhibitors identified Torin-2, which showed an ~18-fold lower IC50 in AXL-knockout than AXL-wildtype cells. PRISM/DepMap analysis confirmed a selective vulnerability to PI3K/AKT/mTOR pathway inhibition, pointing to mTOR inhibition as a therapeutic strategy for AXL-deficient prostate cancer.

  4. nature.com81

    Capillary-selective vasodilation through myosin inhibition halts ischaemic cascades

    Myosin inhibition produces vasodilation that is selective for capillaries and halts the cascades that follow ischaemia, as reported in this work on microvascular obstruction. The approach targets the capillary level, where pericyte-mediated constriction has been linked to no-reflow after ischaemia in the brain, heart and kidney. No quantitative outcome data are reported here.

    Why it matters: It addresses capillary-level no-reflow, a mechanism implicated in stroke, myocardial infarction and kidney injury.

Oct 14Wed
  1. biorxiv.org52

    Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

    Co-targeting KRAS and BCL-2 synergistically triggers GSDME-mediated pyroptosis in KRAS G12D-mutant lung tumors, which are metabolically vulnerable through weakened HK1 interaction and reduced spare respiratory capacity compared with G12C. The combination induces functional tertiary lymphoid structures in vivo, and depletion experiments show the antitumor efficacy depends on B cells. It also drives membrane attack complex deposition in situ and elicits memory antitumor responses.

Oct 13Tue
  1. biospace.com56

    Pfizer pens $500M+ deal with Enodia to destroy disease-causing proteins

    Pfizer has signed a deal with Paris-based Enodia Therapeutics worth up to $500 million, covering an upfront payment plus research, development and sales milestones, with tiered royalties on net sales. Enodia will screen, optimize and develop small-molecule inhibitors of the Sec61 membrane protein complex, while Pfizer handles clinical studies, manufacturing, regulatory and commercial work. Target indications are not yet specified. Pfizer's venture arm had co-led Enodia's €20.7 million ($25 million) seed round in January.

    Why it matters: Pfizer commits over $500 million to a Sec61-targeting platform less than a year after the biotech's launch.

  2. nature.com84

    RevMed’s pancreatic cancer drug first

    The FDA approved Revolution Medicines' Rasonque (daraxonrasib) in August for metastatic pancreatic adenocarcinoma, making it a first-in-class RAS inhibitor for the most common form of pancreatic cancer. Rasonque uses a molecular glue mechanism, binding cyclophilin A and RAS in its GTP-bound 'on' state, unlike KRAS G12C inhibitors such as Lumakras and Krazati. An early-stage trial in September showed promise in lung cancer, raising hopes for use in other hard-to-treat tumors.

    Why it matters: First FDA approval of a pan-RAS inhibitor for metastatic pancreatic adenocarcinoma, with early lung cancer activity.

Oct 10Sat
  1. doi.org49

    JAK-inhibitor treatment induces rapid yet incomplete immune reconstitution in STAT1 gain-of-function

    JAK inhibitors produced rapid but incomplete immune reconstitution in two STAT1 gain-of-function patients carrying p.R321S and p.T385M mutations. Changes were seen as early as 1 week after treatment: T cells rebalanced toward a homeostatic status, TCR repertoire diversity increased quickly, and transcriptional dysregulation in monocytes improved, though defects such as natural killer deficiency persisted in one patient. The work defines both the therapeutic reach and the limits of JAK inhibition in STAT1 GOF.

Oct 9Fri
  1. biorxiv.org48

    Targeting ribosome biogenesis sensitizes PARPi-resistant triple-negative breast cancer

    Inhibiting ribosome biogenesis with BMH-21 resensitizes PARPi-resistant triple-negative breast cancer to olaparib. The drug combination was synergistic in 4 PARPi-resistant cell lines and in 3 BRCA wild-type TNBC cell lines with intrinsic PARPi resistance, but not in parental cells. In MDAMB231 cells, the combination increased γH2AX-positive cells up to 7.3-fold, SA-β-gal staining 5.6-fold and p21 3.6-fold, findings mirrored with CX-5461. Patient cohort data linked ribosomal pathway activity to MYC, proliferation, DNA damage and senescence.

Oct 8Thu
  1. statnews.com40

    STAT+: Roche goes beyond licensing in deal with Chinese biotech

    Roche is partnering with Chinese startup Defand Therapeutics to discover new medicines rather than merely license existing drug candidates, a departure from how pharma companies have approached China in recent years. Defand will discover multiple molecular glue degraders for cancer and immune-driven diseases, drugs designed to attach to problematic proteins and destroy them. Interest in the class grew after Revolution Medicines' molecular glue Rasonque nearly doubled survival in pancreatic cancer patients. Financial terms and next milestones were not disclosed.

  2. biospace.com66

    Big Pharma–backed Matchpoint scores $150M series B, advancing autoimmune asset

    Preclinical Matchpoint Therapeutics has raised a $150 million series B co-led by Nextech Invest and Norwest, with participation from Sanofi Ventures, Atlas Venture, Access Biotechnology and the T1D Fund. The money will advance MPT-062, an oral T cell modulator for autoimmune and inflammatory conditions, into human trials starting next year. Matchpoint also has a July 2025 deal with Novartis, which paid $60 million upfront for its ACE platform and could owe up to $1 billion in milestones plus royalties.

    Why it matters: A large series B funds a first-in-class oral autoimmune program before it reaches human trials, against a market trend favouring later-stage assets.

  3. statnews.com51

    STAT+: Roche inks drug discovery deal with Chinese biotech, focused on molecular glue medicines

    Roche has signed a discovery collaboration with Chinese startup Defand Therapeutics to develop molecular glue medicines for cancer and immune-driven diseases. Financial terms were not disclosed, but a source said the deal could be worth close to $1 billion in upfront fees and milestone payments tied to preclinical, clinical and regulatory goals. Defand will discover and develop multiple drugs under the partnership.

    Why it matters: A big pharma pays a Chinese biotech for discovery-stage molecular glue work rather than late-stage assets.

  4. N Engl J Med40

    Advances in Systemic Treatment of Breast Cancer.

    A New England Journal of Medicine review traces systemic therapy for breast cancer since 2020, covering targeted therapies, antibody-drug conjugates and immunotherapy across biologic subtypes. CDK4/6 inhibitors remain foundational in hormone-receptor-positive, HER2-negative disease, trastuzumab deruxtecan is reshaping HER2-positive treatment, and immune checkpoint inhibitors have improved outcomes in triple-negative breast cancer. Unresolved issues include treatment sequencing, predictive biomarkers, circulating tumor DNA analysis and equitable access to high-cost therapies.

  5. nature.com66

    Molecular glue targets ALK resistance

    Conery et al. report in Nature the discovery and preclinical characterization of TRI-611, a selective, brain-penetrant molecular glue degrader that targets ALK fusion proteins in non-small-cell lung cancer, including tyrosine kinase inhibitor-resistant variants. The approach aims to address acquired resistance driven by ALK kinase domain mutations, TKI toxicity, and limited CNS penetration that hinders treatment of brain metastases. Further preclinical and clinical development would follow.

    Why it matters: Molecular glue degrader offers a new way to overcome ALK TKI resistance and CNS penetration limits in NSCLC.

Oct 7Wed
  1. biocentury.com41

    RougeTx: Reattaching pericytes to stabilize vessels in HHT

    RougeTx, a Naarden, Netherlands-based spinout of Leiden University Medical Center, launched with a $58 million series A co-led by BioGeneration Ventures, Angelini Ventures and Kurma Partners to advance RTX-001 into the clinic. The oral small molecule, designed for once-daily dosing, aims to stabilize blood vessels by reattaching pericytes rather than suppressing angiogenesis in hereditary hemorrhagic telangiectasia. The company will now move RTX-001 toward clinical testing in HHT.

    Why it matters: Series A funds a first-in-class oral approach to a rare vascular disease with no such option named.

Oct 6Tue
  1. biorxiv.org56

    Binding kinetics enable tumor-selective MAPK and growth suppression by a Type 1 RAF Inhibitor

    The Type 1 RAF inhibitor ELV-3111 exploits fast binding dissociation to drive paradoxical MAPK hyperactivation in normal tissues while sparing RAS-mutant tumors, where RAF is already primed. This yields selective MAPK and growth suppression in RAF-dimer-driven models. Combined with a MEK inhibitor, it produced durable regressions in RAS-mutant and BRAF-mutant models, including one refractory to current therapies, with favorable tolerability.

  2. biorxiv.org55

    KRAS-driven metabolic reprogramming of enhanced MFSD2A-mediated lysophosphatidylcholine scavenging promotes survival and progression of pancreatic ductal adenocarcinoma

    Oncogenic KRAS upregulates MFSD2A, driving PDAC cells to scavenge extracellular unsaturated lysophosphatidylcholines and sustain AKT-mediated survival. Plasma lipidomics across 93 newly-diagnosed resectable PDAC cases, 43 chronic pancreatitis patients, and 93 matched controls showed pronounced reductions in circulating LysoPCs associated with PDAC. Blocking MFSD2A or restricting LysoPCs suppressed AKT signaling, increased apoptosis, and slowed tumor growth, and repurposing edelfosine against this axis produced anti-cancer effects in vitro.

  3. biorxiv.org50

    Revisiting AXL as a therapeutic target in soft tissue sarcoma: dubermatinib and bemcentinib effects are largely independent of AXL inhibition

    The AXL inhibitors dubermatinib and bemcentinib reduce viability and induce apoptosis in HT-1080 and SK-LMS-1 soft tissue sarcoma cell models, but shRNA-mediated AXL knockdown fails to reproduce these antiproliferative effects or alter drug sensitivity. Transcriptomic changes induced by the drugs correlate weakly with AXL knockdown, and most drug-regulated genes are AXL-independent. Although STS shows high median AXL mRNA expression in TCGA data, AXL expression was not associated with patient survival, so the rationale for AXL-directed therapy may be reconsidered.

  4. biorxiv.org47

    A Novel ACLY Inhibitor Induces Transcriptional and Metabolic Reprogramming to Overcome Tyrosine kinase inhibitor Resistance in Lymphoma

    The novel ACLY inhibitor VCB1 blocked recombinant human ACLY with an IC of 0.9 uM and suppressed growth of lymphoma cells, retaining potency in TKI-resistant models: 1.62 uM in lorlatinib-resistant SUPM2-LR1000 cells and 0.278 uM in BTK inhibitor-resistant mantle cell lymphoma cells, where the existing inhibitor BMS-303141 was far less active. Multi-omics profiling showed VCB1 suppressed de novo lipogenesis, activated the integrated stress response with induction of ATF4, DDIT3 and related genes, and disrupted nucleotide biosynthesis. The work identifies ACLY as an actionable vulnerability for overcoming TKI resistance in lymphoma.

  5. biorxiv.org47

    A Novel NO Donor 3A72 Activates Mitochondrial-Associated Endoplasmic Reticulum Membrane Structures to Induce Ferroptosis in Triple-Negative Breast Cancer

    The nitric oxide donor 3A72, a furan-coumarin-based compound, suppresses triple-negative breast cancer cell proliferation and restricts xenograft tumor growth, with efficacy matching paclitaxel but with enhanced safety and reduced systemic toxicity. Mechanistically, 3A72 releases NO to cause calcium overload, binds IP3R and ACSL4, and converges on mitochondria-associated ER membranes, where ROS generation couples with lipid remodeling to drive ferroptosis through malondialdehyde accumulation. The findings identify the MAMs calcium-lipid hub as a structural scaffold for antitumor drug development.

Oct 5Mon
  1. biospace.com60

    Lilly doubles down on Gate alliance to unlock new drug class with another $870M+ in biobucks

    Eli Lilly has expanded its alliance with Gate Bioscience in a deal worth up to more than $870 million, adding one new target with the option of a second to their existing collaboration on Gate's Molecular Gate discovery engine for difficult-to-drug extracellular proteins. Gate, which signed an initial deal with Lilly worth up to $856 million in July 2025, will receive an undisclosed upfront payment plus payments on preclinical, clinical and commercial milestones and tiered royalties. Gate leads discovery while Lilly takes an exclusive worldwide license and handles development from later-stage preclinical work through commercialization; no indications have been disclosed.

    Why it matters: Lilly is committing another $870 million to Gate's Molecular Gate platform, deepening a fast-repeat collaboration on a new drug class.

  2. nature.com54

    Oral small-molecule GLP-1RA safiglipron versus dapagliflozin in type 2 diabetes: a randomized, double-blind, active-comparator-controlled phase 3 trial

    Once-daily oral safiglipron, a small-molecule GLP-1RA, was non-inferior to dapagliflozin for HbA1c reduction at all tested doses and superior at 90 mg in adults with type 2 diabetes in a randomized, double-blind, active-comparator-controlled phase 3 trial. Safiglipron gave greater improvements in glycemic control, similar modest weight loss, and an acceptable safety profile. It offers an oral alternative in the GLP-1 receptor agonist class.

    Why it matters: Phase 3 data show an oral GLP-1RA matching and at 90 mg beating dapagliflozin on HbA1c.

Oct 3Sat
  1. nature.com54

    Loss of lineage fidelity underpins drug resistance in Kras -mutant lung cancer

    In genetically engineered mouse models of Kras-mutant lung cancer, lineage fidelity was shown to modulate drug-tolerant residual disease, distinct trajectories of therapeutic resistance, and dependence on oncogenic KRAS. The work points to loss of lineage fidelity as a mechanism underlying the acquired resistance that limits durable clinical responses to KRAS inhibition.

Oct 2Fri
  1. aacrjournals.org80

    In Regulatory First, Myeloma Drug Approved Based on MRD Negativity

    The FDA has approved iberdomide for multiple myeloma on the basis of minimal residual disease negativity, the first approval for the disease to use that endpoint. Iberdomide also represents a new generation of targeted protein degraders, with several more potent cereblon E3 ligase modulators already in clinical development.

    Why it matters: First myeloma approval based on MRD negativity and a new class of cereblon E3 ligase modulators advancing.

Oct 1Thu
  2. biospace.com54

    Foghorn lays off 40% of staff after Lilly collaboration ends

    Foghorn Therapeutics and Eli Lilly ended their oncology collaboration after Phase 1 data on cancer candidate FHD-909 (LY4050784) showed insufficient efficacy, halting its move into clinical development expansion and a SMARCA2 degrader program. Foghorn is cutting about 40% of its workforce, leaving roughly 65 full-time employees, and will refocus on its proprietary programs including EP300 and CBP degraders. The 2021 deal had brought $300 million upfront plus an $80 million equity investment from Lilly's Loxo Oncology, and the changes should extend Foghorn's cash runway into the second half of 2029.

    Why it matters: A terminated big-pharma oncology alliance triggers pipeline reprioritization, layoffs and a readout on the SMARCA2 synthetic lethality hypothesis.

  3. Nat Med53

    Oral small-molecule GLP-1 receptor agonist safiglipron in early type 2 diabetes: a randomized, double-blind, placebo-controlled trial.

    Once-daily oral safiglipron reduced HbA1c by 1.20 to 1.45 percentage points versus placebo at 32 weeks in 284 adults with early type 2 diabetes managed with diet and exercise alone (OUTSTAND-1, phase 3). HbA1c below 7.0% was reached by 71.4-77.8% of safiglipron recipients versus 25.0% on placebo, with modest weight loss and mostly mild or moderate gastrointestinal adverse events. It offers an oral GLP-1 receptor agonist option taken without fasting or dietary restrictions.

    Why it matters: Phase 3 evidence that an oral small-molecule GLP-1 receptor agonist matches injectable-class glycemic efficacy.

  4. Nat Med60

    Werner helicase inhibitor for advanced microsatellite instability solid tumors: a phase 1 trial.

    RO7589831 (VVD-133214), a first-in-class covalent inhibitor of Werner syndrome helicase, showed manageable safety and early antitumor activity in 88 patients with MSI and/or mismatch repair-deficient advanced solid tumors in part 1 of a phase 1 trial. TEAEs were mostly grade 1-2, with no grade 5 events and discontinuation in 3.4% (3/88). In 66 MSI efficacy-evaluable patients, disease control rate was 74.2%, objective response rate 10.6% (7 partial responses), median PFS 6.7 months and median OS 17.6 months; 150 mg and 600 mg BID were selected as recommended phase 2 doses.

    Why it matters: First-in-human data on a WRN covalent inhibitor, a synthetic lethal target for MSI cancers.

  5. biorxiv.org41

    The Smac mimetic drug Xevinapant sensitizes triple negative breast cancer to radiotherapy-induced cell death in a TNFα dependent manner

    The Smac mimetic Xevinapant (AT406) sensitized triple-negative breast cancer cell lines to radiotherapy-induced cell death in vitro, with clonogenic assays in MDA-MB-231 cells showing a dose-enhancing factor of 1.57. Radiosensitization was significantly enhanced by TNF and mediated by TNF-dependent apoptosis, assessed by western blotting, flow cytometry and cell cycle analysis. The findings support combining radiotherapy with Xevinapant to improve local control in TNBC.

  6. medrxiv.org46

    Axitinib in Progressive Metastatic Pheochromocytoma and Paraganglioma: Results of a Phase II Study

    Single-agent axitinib produced confirmed partial responses in 35.3% of 17 treated patients with progressive metastatic or unresectable pheochromocytoma and paraganglioma, with median progression-free survival of 7.9 months and median overall survival of 29 months. Hypertension occurred in 79% of patients but was managed with antihypertensive therapy and dose modification, and no patient stopped treatment for toxicity. The phase II trial's efficacy compares favorably with sunitinib in this rare disease.

    Why it matters: First prospective single-arm data on selective VEGFR inhibition with axitinib in a rare cancer with few systemic options.

  7. nature.com61

    GPCR antagonism via rewiring of receptor trafficking and degradation

    Bifunctional antibodies termed GTACs, which bind both a GPCR and the constitutively internalizing transferrin receptor 1, drive receptor endocytosis and lysosomal degradation, silencing signalling instead of competing with ligands. GTACs depleted and antagonized AT1R, RXFP1, CCR6 and BILF1, blocking chemotaxis in primary immune cells, suppressing angiotensin-potentiated contraction in iPSC-derived cardiomyocytes and inhibiting constitutive BILF1 signalling. GTACs showed more than 10-100-fold greater potency and improved efficacy over conventional antagonists, and the approach extended to APJ, A2AR and M3R.

    Why it matters: Offers a degradation-based alternative for GPCRs that resist classical competitive antagonism.

Sep 30Wed
  1. biorxiv.org51

    Dual inhibition of p38α MAPK and Casein kinase δ/ϵ as a novel treatment strategy for AR-independent and taxane-resistant advanced prostate cancer

    TAK-715, a dual inhibitor of p38 MAPK and Casein kinase δ/ε, showed efficacy against metastatic castration-resistant prostate cancer (mCRPC), including taxane-resistant lines and a highly aggressive metastatic variant, as a single agent and combined with taxanes. Its apoptotic effects occur via a mitochondrial-mediated pathway, and pathway analysis of bulk tumor RNA sequencing pointed to mitochondrial dysfunction and cell cycle arrest as top networks, with HES1 the top differentially expressed gene. Single-cell transcriptomics showed TAK-715 erodes subclonal populations driving cancer stemness, metastasis, and drug resistance, with findings validated in silico across multiple patient datasets.

  2. endpoints.news41

    Merck licenses a KRAS G12D inhibitor for $400M upfront

    Merck is licensing a KRAS G12D inhibitor from entrepreneur and synthetic chemist Tao Hu for $400 million upfront. Hu previously sold a different KRAS G12D inhibitor to AstraZeneca in 2023. Terms beyond the upfront payment and next steps were not disclosed.

    Why it matters: Large upfront licensing deal for a KRAS G12D inhibitor by a repeat seller of such assets.

Sep 29Tue
  1. statnews.com43

    STAT+: AstraZeneca invests $2 billion in Summit Therapeutics

    AstraZeneca has invested $2 billion in Summit Therapeutics, according to the headline of a STAT+ report. Separately, Novo Nordisk licensed a once-weekly oral GLP-1/GIP receptor agonist for obesity from Hengrui Pharma, paying $300 million upfront for global rights outside China, with total deal value of $2.6 billion if milestones are met; the drug is ready for Phase 1 development.

    Why it matters: AstraZeneca's $2 billion Summit stake and Novo's $2.6 billion obesity drug deal both move competitive pharma positioning.

  2. biospace.com45

    Novo adds long-term obesity differentiation in up to $2.6B Hengrui deal

    Novo Nordisk is licensing HRS-1596, Hengrui Pharma's once-weekly oral GLP-1R/GIPR dual agonist ready for Phase 1, paying $300 million upfront with the deal worth up to $2.6 billion in milestones plus royalties. The asset is intended for obesity, type 2 diabetes and other metabolic diseases, and China has already cleared it for a Phase 1 study in weight management and T2D. BMO Capital Markets says the deal is unlikely to change near-term competition but once-weekly oral dosing could offer longer-term differentiation.

  3. biorxiv.org53

    SMYD3 protein degraders in HPV-negative head and neck squamous cell carcinoma.

    SMYD3 PROTACs, unlike catalytic inhibitors that lack phenotypic efficacy, degrade SMYD3 and curb proliferation and invasion in HPV-negative HNSCC cell lines. The compound IAP-08 degrades SMYD3 with a DC50 of about 177 nM and Dmax of about 90%, forms ternary complexes with XIAP E3 ligase, and shows favorable pharmacokinetics in vivo. Degradation, but not enzymatic inhibition, reprograms cell cycle, EMT and type I IFN response genes, supporting clinical development of IAP-08 in a disease where SMYD3 is overexpressed in about 60% of tumors.

    Why it matters: It reframes SMYD3 as undruggable by inhibitors alone and provides a degrader with in vivo feasibility for HPV-negative HNSCC.

  4. nature.com47

    Psychedelic protects against chemotherapy-induced nerve damage

    Pretreatment with the psychedelic drug psilocybin prevented chemotherapy-induced peripheral neuropathy in preclinical models. The work, reported in Science by Heles and colleagues, links the effect to preservation of mitochondrial trafficking, a mechanism damaged by platinum-based chemotherapy. The finding points to a way to protect against this dose-limiting adverse effect without altering the chemotherapy itself.

    Why it matters: A psychedelic drug prevented chemotherapy-induced peripheral neuropathy in preclinical models by preserving mitochondrial trafficking.

  5. nature.com54

    A synthetic lethal drug for microsatellite instability cancers

    Inhibition of the Werner syndrome helicase (WRN) enzyme exploits a new synthetic lethal vulnerability in cancers with microsatellite instability, a phase 1 trial shows. The approach offers a new way to target these tumors beyond immune checkpoint inhibition. No efficacy numbers are reported in the material.

    Why it matters: First clinical evidence that WRN inhibition can target microsatellite instability cancers beyond checkpoint inhibitors.

  6. BioCentury68

    Merck turns to China-based SciBrunch for KRAS program, pays $400M up front: Deals Report

    Merck & Co. has licensed global rights to SPR2015, a preclinical KRAS G12D molecular glue inhibitor from China-based SciBrunch, paying $400 million up front. The deal follows reported failed M&A negotiations with Revolution Medicines in the $30 billion range, after that company reported in April that daraxonrasib led to a survival benefit in pancreatic cancer patients. Further deal terms for the SciBrunch agreement were not disclosed.

    Why it matters: Large upfront licensing payment by Merck for a preclinical KRAS G12D program after failed Revolution Medicines talks.

Sep 28Mon
  1. biospace.com45

    Merck inks up to $2.13B deal to dine with SciBrunch, gain rights to preclinical KRAS inhibitor

    Merck has licensed exclusive global rights to SciBrunch Therapeutics' preclinical oral KRAS G12D (ON) inhibitor SPR2015, paying $400 million upfront with milestone payments that could bring the total to $2.13 billion. The deal has closed, and Merck recorded a pre-tax charge of $400 million, about 13 cents per share, in Q3. SciBrunch expects SPR2015 to enter human trials by the end of this year. The same day, Merck and Daiichi Sankyo withdrew an accelerated approval request for ifinatamab deruxtecan in extensive-stage small cell lung cancer after the FDA said the data did not support the filing.

    Why it matters: Large licensing deal for a preclinical KRAS G12D inhibitor plus a withdrawn FDA filing shapes Merck's oncology pipeline.

CBACBA Frontier Insights (CFI)Chinese Biopharmaceutical Association (CBA)www.cba-usa.org