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Elisrasib

May 11, 2026 2:30 am / Leave a comment

Elisrasib

CAS2914919-85-8

MFC32H35F6N7O3. MW 679.7 g/mol

2-[(2S)-4-[(7S)-7-[3-amino-2-fluoro-5-methyl-6-(trifluoromethyl)phenyl]-2-[[(2R,8S)-2-fluoro-1,2,3,5,6,7-hexahydropyrrolizin-8-yl]methoxy]-7,8-dihydro-5H-pyrano[4,3-d]pyrimidin-4-yl]-1-(2-fluoroprop-2-enoyl)piperazin-2-yl]acetonitrile

[(2S)-4-[(7S)-7-[3-amino-2-fluoro-5-methyl-6-(trifluoromethyl)phenyl]-2-{[(2R,7aS)-2-fluorotetrahydro-1Hpyrrolizin-7a(5H)-yl]methoxy}-7,8-dihydro-5H-pyrano[4,3-d]pyrimidin-4-yl]-1-(2-fluoroprop-2-enoyl)piperazin-2-yl]acetonitrile
Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, D3S 001, PFW9YLB86H

Elisrasib (D3S-001) is a next-generation, orally available KRAS G12C inhibitor developed by D3 Bio that demonstrates high potency, sustained target engagement, and strong clinical activity in advanced solid tumors, including those resistant to first-generation inhibitors. As of April 2026, clinical trials show it has a 52% objective response rate (ORR) in G12C inhibitor-naive patients and a 30% ORR in refractory populations.

Key Aspects of Elisrasib (D3S-001):

Mechanism of Action: It is a highly potent, covalent inhibitor that selectively binds the GDP-bound (inactive) form of the KRAS G12C mutant, effectively halting tumor cell proliferation and metastasis.
Superior Efficacy: Preliminary data suggests elisrasib may be more potent than earlier inhibitors like sotorasib and adagrasib, providing higher target occupancy at lower doses.
Clinical Performance (AACR 2026 Data):
- Naive Patients: 52% ORR, with a median duration of response (mDOR) of 16.5 months and median progression-free survival (mPFS) of 12.2 months at the 600 mg dose.
- Refractory Patients: 32% ORR, with a mDOR of 15.6 months and mPFS of 8.1 months.
Targeted Cancers: Clinical trials are focused on KRAS G12C-mutant tumors, specifically non-small cell lung cancer (NSCLC), colorectal cancer (CRC), and other solid tumors.
Safety Profile: The drug has shown good tolerability and a safe profile in early studies.

Elisrasib is in Phase 1/2 development and was highlighted for its promising results in treating patients with KRAS G12C-mutant tumors

Elisrasib is an orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, elisrasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.

A Phase 1 Study to Assess Food Effect on the Pharmacokinetics of D3S-001 in Healthy Adult ParticipantsCTID: NCT07093398Phase: Phase 1Status: CompletedDate: 2026-03-25
A Phase 1/2 Study of D3S-002 as Monotherapy or Combination Therapy in Adult Subjects With Advanced Solid Tumors With MAPK Pathway MutationsCTID: NCT05886920Phase: Phase 1/Phase 2Status: Active, not recruitingDate: 2026-03-23
A Study of D3S-001 Monotherapy or Combination Therapy in Subjects With Advanced Solid Tumors With a KRAS p.G12C MutationCTID: NCT05410145Phase: Phase 1/Phase 2Status: RecruitingDate: 2026-03-12

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2025171055&_cid=P22-MP0KTH-20644-1

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=US398107452&_cid=P22-MP0KWU-22960-1

Example 17

Step 6: Synthesis of Compound 17

Dichloromethane (5 mL) was added to a dry reaction flask, and then compound 17-6 (50 mg, 82.29 μmol, 1 eq), 2-fluoroacrylic acid (14.82 mg, 164.58 μmol, 2 eq), and N,N-diisopropylethylamine (31.90 mg, 246.87 μmol, 43.00 μL, 3 eq) were added. The mixture was stirred. The reaction system was cooled down to −60° C. and O-(7-azabenzotriazol-1-yl)-N,N,N,N-tetramethyluronium hexafluorophosphate (37.55 mg, 98.75 μmol, 1.2 eq) was added. The mixture was then stirred for 0.5 h. The mixtures were combined for treatment. The reaction mixture was quenched by adding water (5 mL) to the reaction solution and the layers were separated. The organic phase was dried with anhydrous sodium sulfate and filtered. The filtrate was concentrated under reduced pressure to give a crude product, which was purified by a high-performance liquid chromatography column {column: Welch Xtimate C18 100*25 mm*3 μm; mobile phase: [H ₂O(0.05% HCl)-ACN]; acetonitrile %: 20%-50%, 8 min} to give compound 17. SFC analysis method (column: Chiralcel OD-3, 50×4.6 mm I.D., 3 μm; Mobile phase: A (CO2) and B (methanol, containing 0.05% diisopropylamine); Gradient: B %=5-50%, 3 min; Flow rate: 3.4 mL/min; Wavelength: 220 nm; Pressure: 1800 psi, Optical purity: 99.21%, time-to-peak: 1.840). ¹H NMR (400 MHz, CD ₃OD) δ=6.80-6.68 (m, 1H), 5.73-5.51 (m, 1H), 5.46-5.19 (m, 3H), 5.05-4.90 (m, 3H), 4.74-4.58 (m, 2H), 4.37-4.26 (m, 1H), 4.20-4.06 (m, 2H), 4.05-3.84 (m, 3H), 3.79-3.59 (m, 2H), 3.54-3.43 (m, 1H), 3.42-3.35 (m, 1H), 3.31-3.24 (m, 1H), 3.13-2.89 (m, 3H), 2.82-2.52 (m, 2H), 2.50-2.42 (m, 1H), 2.41-2.30 (m, 5H), 2.29-2.18 (m, 1H).

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References

Pyrimidoheterocyclic compounds and application thereofPublication Number: EP-4105211-A1Priority Date: 2020-03-12
Pyrimidoheterocyclic compounds and application thereofPublication Number: US-2023151004-A1Priority Date: 2020-03-12

//////////elisrasib, anax labs, Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, D3S 001, PFW9YLB86H

Elironrasib

May 9, 2026 2:36 am / Leave a comment

Elironrasib

CAS 2641998-63-0

MFC55H78FN9O8 MW 1012.3 g/mol

1-[4-(dimethylamino)-4-methylpent-2-ynoyl]-N-[(2S)-1-[[(6S,8S,14S)-22-ethyl-21-[2-[(1S)-1-methoxyethyl]-3-pyridinyl]-18,18-dimethyl-9,15-dioxo-5,16-dioxa-2,10,22,28-tetrazapentacyclo[18.5.2.1^2,6.1^10,14.0^23,27]nonacosa-1(26),20,23(27),24-tetraen-8-yl]amino]-3-methyl-1-oxobutan-2-yl]-4-fluoro-N-methylpiperidine-4-carboxamide

Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6291, RMC 6291, 942KVV5CJP

Elironrasib (RMC-6291) is an investigational, orally bioavailable, RAS(ON) G12C-selective inhibitor developed by Revolution Medicines that targets the active GTP-bound form of KRAS G12C. In Phase 1 trials, it showed significant promise in treating advanced KRAS G12C-mutated solid tumors, including non-small cell lung cancer (NSCLC). [1, 2, 3]

Key Clinical Trial Results (as of Oct 2025):

Response Rate: 42% objective response rate (ORR).
Disease Control: 79% disease control rate (DCR).
Durability: Median duration of response was 11.2 months.
Survival: Median progression-free survival was 6.2 months.
Overcoming Resistance: Demonstrated efficacy in patients who had previously progressed on first-generation KRAS G12C(OFF) inhibitors.

Mechanism of Action:
Elironrasib acts as a covalent tri-complex inhibitor (TCI). It forms a complex with the intracellular chaperone protein cyclophilin A (CypA) and the active KRAS G12C(GTP) protein, effectively shutting down oncogenic signaling.

Development Status:

Designation: It has received FDA breakthrough therapy designation for KRAS G12C-mutant NSCLC.
Trials: Currently in Phase 1 clinical trials (e.g., NCT05462717) to evaluate safety, tolerability, and efficacy, both as a monotherapy and in combination.
Target Population: Patients with KRAS G12C-addicted solid tumors.

Discovery of Elironrasib (RMC-6291), a Potent and Orally Bioavailable, RAS(ON) G12C-Selective, Covalent Tricomplex Inhibitor for the Treatment of Patients with RAS G12C-Addicted Cancers – PubMed27 Mar 2025 — This information does not constitute medical advice or diagnosis. Elirronrasib (RMC-6291) is a potent, orally bioavailable,

Revolution Medicines to Present Updated Elironrasib Safety and Efficacy Data in Patients with KRAS G12C Non-Small Cell Lung Cancer Following Treatment with a KRAS(OFF) G12C Inhibitor22 Oct 2025 — This information does not constitute medical advice or diagnosis. Elirronrasib is a RAS(ON) G12C-selective inhibitor being develop…Revolution Medicines
Elironrasib May Overcome Resistance to Prior KRAS G12C Inhibition in Non-small Cell Lung Cancer

OriginatorREVOLUTION Medicines
ClassAntineoplastics; Morpholines; Piperidines; Pyridazines; Small molecules
Mechanism of ActionKRAS protein inhibitors
Phase I/IISolid tumours
Clinical Phase UnknownNon-small cell lung cancer
30 Jan 2026Phase-I/II clinical trials in Solid tumours (Combination therapy, Late-stage disease, Metastatic disease) in USA (PO) (NCT07397338)
31 Oct 2025Elironrasib is still in phase I trial in Solid tumours (Late-stage disease, Metastatic disease, Monotherapy) in Australia, Italy, South Korea, Malaysia, Singapore, Spain, Czech Republic, Thailand and USA (PO, Tablet) (NCT05462717)
28 Oct 2025No recent reports of development identified for phase-I development in Solid-tumours(Late-stage disease, Metastatic disease, Monotherapy) in Australia, Italy, South Korea, Malaysia, Singapore, Spain, Czech Republic, Thailand (PO, Tablet)

Elironrasib is an orally bioavailable, covalent inhibitor of the active, guanosine triphosphate (GTP)-bound form of the oncogenic KRAS substitution mutation G12C, KRAS G12C(ON), with potential antineoplastic activity. Upon oral administration, elironrasib forms a tri-complex with the intracellular chaperone protein and immunophilin cyclophilin A (CypA) and KRAS G12C(ON). This tri-complex inhibits KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.

Study of Elironrasib and Daraxonrasib as Monotherapies and Combination Therapy in Participants With Advanced KRAS G12C Mutant Solid TumorsCTID: NCT06128551Phase: Phase 1/Phase 2Status: RecruitingDate: 2026-04-23
Dose Escalation and Dose Expansion Study of RMC-6291 Monotherapy in Subjects With Advanced KRASG12C Mutant Solid TumorsCTID: NCT05462717Phase: Phase 1Status: Active, not recruitingDate: 2026-04-08
Study of RAS(ON) Inhibitors in Combination With Ivonescimab in Patients With Solid TumorsCTID: NCT07397338Phase: Phase 1/Phase 2Status: RecruitingDate: 2026-03-30
Study of RAS(ON) Inhibitors in Patients With Advanced RAS-mutated NSCLCCTID: NCT06162221Phase: Phase 1/Phase 2Status: RecruitingDate: 2026-03-09

SYN

https://pubs.acs.org/doi/10.1021/acs.jmedchem.4c02313

SYN

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2023205701&_cid=P10-MOXQ72-19496-1

PAT’

https://patentscope.wipo.int/search/en/detail.jsf?docId=US443002383&_cid=P10-MOXQ72-19496-1

Part 5—Synthesis of Compound A—(1²M)-1-(4-(dimethylamino)-4-methylpent-2 ynoyl)-N-((2S)-1-(((2²S,6³S,4S)-1¹-ethyl-12-(2-((S)-1-methoxyethyl)pyridin-3-yl)-10,10-dimethyl-5,7-dioxo-6¹,6²,6³,6⁴,6⁵,6⁶-hexahydro-1¹H-8-oxa-2(4,2)-morpholina-1(5,3)-indola-6(1,3) pyridazinacycloundecaphane-4-yl)amino)-3-methyl-1-oxobutan-2 yl)-4-fluoro-N-methylpiperidine-4-carboxamide

To a 50 L glass reactor was charged Compound 15 (1.91 kg, 1.0 eq) and DMF (13.9 kg). The mixture was agitated at 20-30° C. until all of the solids were dissolved. Compound 2 (1.70 kg, 1.2 eq) and DMF (3.8 kg) were charged. The mixture was agitated at 20-30° C. until all of the solids were dissolved. DIPEA (2.20 kg, 5.50 eq) was charged at 20-30° C. and the mixture was cooled to −20-−10° C. under agitation. Ethyl cyanoglyoxylate-2-oxime (Oxyma) (0.48 kg, 1.1 eq) was charged to the reactor and the reaction mixture was agitated at −20 to −10° C. for 30 min. PyBOP was charged as a DMF solution (1.89 kg dissolved in 3.62 kg DMF, 1.2 eq) to the reactor at −20 to −10° C. in </=1 h. The reaction mixture was agitated at −20 to −10° C. for 1-3 h. Reaction monitoring by HPLC showed the reaction was complete.

The crude reaction mixture was diluted with EtOAc (3.6 kg) and partitioned with a mixture of EtOAc (65 kg) and brine (25 wt %, 132 kg). The biphasic mixture was agitated at 20-30° C. for 1 h and filtered through a pad of diatomite. EtOAc (11 kg) was used to rinse the reactor and spent filter aid wet cake. The combined filtrates were allowed to stand for 1 h before the phases were separated. The organic layer was washed once with brine (25 wt %, 90 kg×2). HCl (0.6 M aqueous solution, 71 kg) was charged to the isolated organic layer at 5-20° C. The biphasic mixture was agitated at 10-20° C. for 1 h. The phases were separated, and the upper lean organic phase was extracted with HCl (0.6 M aqueous solution, 30 kg). The combined rich aqueous phases were washed three times with EtOAc (34 kg×3). To the washed aqueous phase was charged EtOAc (34 kg) and the pH was adjusted to pH 9-10 by charging Na ₂CO ₃aqueous solution (30 wt %) at 10-20° C. The mixture was agitated at 10-20° C. for 1 h and the phases were separated. The lean aqueous phase was extracted with EtOAc (34 kg), and the combined rich organic phases were washed twice with brine (25 wt %, 90 kg×2). The resulting organic layer was then washed with a solution of acetic acid in brine (prepared by dissolving 0.23 kg glacial acetic acid and 8 kg 25 wt % brine in 115 kg water) (39 kg×2), a solution of Na ₂CO ₃in brine (prepared by dissolving 1.3 kg Na ₂CO ₃and 8 kg 25 wt % brine in 31 kg water) (40 kg), and brine (25 wt %, 92 kg), respectively. The crude organic solution was then treated with CUNO® by filtering through a cartridge and the filtrate was concentrated under reduced pressure at NMT 40° C. to ˜30 L. The crude residue was then crystallized by charging n-heptane (57 kg) with seed (0.040 kg).

The crude product was then further purified by recrystallization with a mixture of EtOAc and n-Heptane to give purified Compound A as a white solid.

HRMS (ESI+)Calculated for C₅₅H₇₈FN₉O₈(M+H): 1012.6036Found: 1012.6065

1H NMR (400 MHz, CD ₃OD, 23° C.)δ8.71 (dd J=4.8, 1.6 Hz, 1H), 7.83 (d, J=7.2 Hz, 1H), 7.50 (dd, J=8.0, 4.8 Hz, 1H), 7.39 (d, J=8.0 Hz, 1H), 7.11 (s, 1H), 7.07 (dd, J=9.0, 2.0 Hz, 1H), 5.67 (d, J=8.8 Hz, 1H), 4.62 and 4.52 (d, J=10.0 Hz, 1H, as rotamers), 4.46 (d, J=12.4 Hz, 1H), 4.28-4.37 (m, 2H), 4.24 (q (J=6.4 Hz, 1H), 4.12-4.17 (m, 1H), 3.50-4.00 (m, 9H), 3.28 (d, J=10.8 Hz, 1H), 3.10-3.20 and 2.90-3.00 (m, 8H, as rotamers), 2.60-2.80 (m, 4H), 2.35 (s, 3H), 2.34 (s, 3H), 2.05-2.35 (m, 7H), 1.85-1.95 (m, 2H), 1.60-1.73 (m, 2H), 1.46 (s, 3H), 1.45 (s, 3H), 1.44 (s, 3H), 0.96 and 1.02 (d, J=6.4 Hz, 3H, as rotamers), 1.00-1.10 (m, 3H), 0.83 and 0.87 (dd, J=6.8, 2.0 Hz, 3H, as rotamers), (0.77 (bs, 3H), 0.64 (bs, 3H)

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References

Macrocyclic heterocycles and uses thereofPublication Number: US-2023339952-A1Priority Date: 2022-04-20
Macrocyclic heterocycles and uses thereofPublication Number: WO-2023205701-A1Priority Date: 2022-04-20
Methods for delaying, preventing, and treating acquired resistance to ras inhibitorsPublication Number: US-2023233569-A1Priority Date: 2020-06-18
Ras inhibitorsPublication Number: US-2021130303-A1Priority Date: 2019-11-04
Ras inhibitorsPublication Number: US-2023234929-A1Priority Date: 2019-11-04
Ras inhibitors
Publication Number: US-11566007-B2
Priority Date: 2019-11-04
Grant Date: 2023-01-31

////////elironrasib, ANAX LABS, Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6291, RMC 6291, 942KVV5CJP

Daraxonrasib

April 25, 2026 2:29 am / Leave a comment

Daraxonrasib

CAS 2765081-21-6

MFC44H58N8O5S MW811.0 g/mol

trans-(1S,2S)-N-[(7S,13S)-21-ethyl-20-[2-[(1S)-1-methoxyethyl]-5-(4-methylpiperazin-1-yl)-3-pyridinyl]-17,17-dimethyl-8,14-dioxo-15-oxa-4-thia-9,21,27,28-tetrazapentacyclo[17.5.2.1^2,5.1^9,13.0^22,26]octacosa-1(25),2,5(28),19,22(26),23-hexaen-7-yl]-2-methylcyclopropane-1-carboxamide

Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2,

Daraxonrasib (formerly RMC-6236) is an investigational, orally administered “molecular glue” RAS inhibitor developed by Revolution Medicines for treating advanced solid tumors with RAS mutations, particularly metastatic pancreatic cancer. April 2026 Phase 3 trials showed it significantly improves survival, demonstrating high potential as a first-line treatment.

Key Clinical Findings and Updates (as of April 2026):

Mechanism: It acts as a RAS(ON) inhibitor, targeting mutated and wild-type RAS proteins () to disrupt cancer signaling.
Breakthrough Results: Data from the RASolute 302 trial showed a substantial survival benefit in patients with previously treated metastatic pancreatic ductal adenocarcinoma (PDAC).
High Response Rates: In trials, daraxonrasib combined with chemotherapy showed a 58% confirmed objective response rate (ORR) and 84% progression-free survival (PFS) at 6 months in untreated RAS-mutant metastatic pancreatic cancer.
Safety Profile: Generally well-tolerated, with side effects including rash, diarrhea, stomatitis, and nausea.
Recognition: Named the “2025 Molecule of the Year” by Drug Hunter for its, novel mechanism and clinical potential.

Daraxonrasib is currently being studied in the Phase 3 RASolute 303 trial for first-line treatment of pancreatic cancer.

Daraxonrasib (RMC-6236) is a RAS inhibitor drug. It is undergoing testing by Revolution Medicines to treat advanced solid tumors with RAS mutations, especially metastatic pancreatic ductal adenocarcinoma (PDAC) containing KRAS G12X mutations.^[1] It received a breakthrough therapy designation from the U.S. Food and Drug Administration.^[2]

Daraxonrasib is orally active and multi-selective RAS inhibitor. It uses a tri-complex mechanism to target the active, GTP-bound form of RAS proteins, including mutant and wild-type forms. Unlike conventional RAS inhibitors, it first binds to the chaperone-like protein cyclophilin A to form a complex, which then attaches to active RAS. This interaction blocks downstream effector binding and inhibits oncogenic signaling.^[3]

In 2026, Daraxonrasib clinical trial completed a phase 3 clinical trial (RASolute 302) to assess efficacy compared to standard-of-care chemotherapy.^[4] The trial met all primary and key secondary endpoints, including progression-free survival (PFS). The company reported median survival of 13.2 months with daraxonrasib vs. 6.7 months with standard chemotherapy. The hazard ratio for death was 0.40 (a 60% reduction in risk of death; p < 0.0001). Daraxonrasib was generally well tolerated with a manageable safety profile and no new safety signals.^[5]

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2024216048&_cid=P20-MODPOO-66335-1

PAT

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2024216017&_cid=P20-MODPOO-66335-1

PATENT ATTORNEY DOCKET: 51432-038WO2 Part 4 – Purification of Compound A – (1S,2S)-N-[(7S,13S)-21-ethyl-20-{2-[(1S)-1- methoxyethyl]-5-(4-

1.0equiv) at 25°C. The resulting suspension was stirred until solids were completely dissolved. The resulting methanol solution was filtered through microporous filter and transferred to another reactor. Then the reactor temperature was maintained at 25°C and slowly water (2.41kg, 1.0 V) water was added over a period of 30 minutes. The resulting cloudy solution was stirred for another 30 minutes at 25°C. Then a solution of methanol and water (3.42kg, 1:2, v/v) slowly over 1 hour. The resulting suspension was stirred for 2 hours at 25°C. Again, to the suspension additional water (2.48kg) slowly added over 1 hour. The final, suspension was stirred for additional 1 hour. Water (9.29kg, 3.75 V) was added to the suspension slowly over 2 hours and the mixture was stirred for at least for 16 hours at 25°C. The resulting suspension was filtered and washed with mixed solvent water: MeOH (3:2, v/v) twice (2x 2.2 kg), followed by water (4.91kg) washing. The wet cake was dried under reduced pressure and controlled humidity (temperature: 25 ± 5 ˚C, vacuum ≥ -0.085 MPa, humidity: 10%~20%) for 37 hours to afford Compound A as a white solid (2.68 kg, 99.4% a/a purity, 93.0% w/w assay, KF: 6.7%, 3.07 mol, 92% yield, Table 27).

PAT

Synthesis of ras inhibitorsPublication Number: WO-2024216017-A2Priority Date: 2023-04-14
Macrocycle compounds useful as kras inhibitorsPublication Number: WO-2024008834-A1Priority Date: 2022-07-08
Ras inhibitorsPublication Number: US-11690915-B2Priority Date: 2020-09-15Grant Date: 2023-07-04
Ras inhibitorsPublication Number: US-2023226186-A1Priority Date: 2020-09-15

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References

Cregg J, Edwards AV, Chang S, Lee BJ, Knox JE, Tomlinson AC, et al. (March 2025). “Discovery of Daraxonrasib (RMC-6236), a Potent and Orally Bioavailable RAS(ON) Multi-selective, Noncovalent Tri-complex Inhibitor for the Treatment of Patients with Multiple RAS-Addicted Cancers”. Journal of Medicinal Chemistry. 68 (6): 6064–6083. doi:10.1021/acs.jmedchem.4c02314. PMID 40056080.
Sava J (July 1, 2025). “Daraxonrasib Earns FDA Breakthrough Status in Pancreatic Cancer”. Targeted Oncology. Retrieved October 12, 2025.
Jiang J, Jiang L, Maldonato BJ, Wang Y, Holderfield M, Aronchik I, et al. (June 2024). “Translational and Therapeutic Evaluation of RAS-GTP Inhibition by RMC-6236 in RAS-Driven Cancers”. Cancer Discovery. 14 (6): 994–1017. doi:10.1158/2159-8290.CD-24-0027. PMC 11149917. PMID 38593348.
Clinical trial number NCT05379985 at ClinicalTrials.gov
Mast J (2026-04-13). “Revolution Medicines touts ‘unprecedented’ data for pancreatic cancer pill”. STAT. Retrieved 2026-04-13.

Clinical data

Other names	RMC-6236
Identifiers
IUPAC name
CAS Number	2765081-21-6
PubChem CID	164726578
IUPHAR/BPS	13368
ChemSpider	115275938
UNII	B6T47Y2UAP
KEGG	D13265
ChEBI	CHEBI:746946
Chemical and physical data
Formula	C₄₄H₅₈N₈O₅S
Molar mass	811.06 g·mol⁻¹
3D model (JSmol)	Interactive image
SMILES
InChI

//////////daraxonrasib, anax labs, Kirsten rat sarcoma viral oncogene homolog inhibitor, antineoplastic, RMC-6236, RMC 6236, B6T47Y2UAP, RAS-IN-2,

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Step 6: Synthesis of Compound 17

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