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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
49 Results for "
KRAS-G12C mutant
" in MedChemExpress (MCE) Product Catalog:
Products (49)
49 Results for "KRAS-G12C mutant" in MCE Product Catalog:
18
18 Publications Verification
RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (Kd = 195 nM) and KRAS (G12V) (Kd = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRAS G12C cancer models, and demonstrates good tolerability across various RAS cancer models .
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5 Cited Publications
Cat. No.: HY-19706
CAS No.: 1629268-00-3
ARS-853 is a cell-active, selective, covalent KRAS G12C inhibitor with an IC50 of 2.5 μM. ARS-853 inhibits mutant KRAS-driven signaling by binding to the GDP-bound oncoprotein and preventing activation .
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Elironrasib is an orally active and covalent inhibitor of KRAS G12C(ON). Elironrasib forms a tri-complex within tumor cells between KRAS G12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRAS G12C(ON) from signaling via steric blockade of RAS effector binding. Elironrasib inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. Elironrasib also inhibits the proliferation of KRAS G12C mutant cells with a median IC50 of 0.11 nM .
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2 Cited Publications
LC-2 is an orally active PROTAC-class degrader targeting KRAS G12C and a MAPK inhibitor. LC-2 shows higher selectivity for KRAS G12C than wild-type KRAS and other KRAS mutants. LC-2 covalently binds to KRAS G12C via the MRTX849 (HY-130149) warhead, recruits the VHL E3 ligase to form a ternary complex, and induces ubiquitination and degradation of KRAS G12C. Meanwhile, LC-2 inhibits the MAPK signaling pathway, reduces the phosphorylation levels of CRAF and AKT, thereby inducing apoptosis and suppressing cancer cell and tumor growth. LC-2 can be used for the research of KRAS G12C-positive cancers, including non-small cell lung cancer and colorectal cancer .
1
1 Cited Publications
Synonyms: AMG-510 racemate
Sotorasib racemate (Compound A) is an orally active racemate of Sotorasib (HY-114277), a covalent inhibitor of KRAS G12C mutant which induces adaptive feedback activation of MAPK pathway. Sotorasib racemate also exerts inhibitor activity against KRAS G12C induced cancer and can be applied to cancer research .
1
1 Cited Publications
KRAS inhibitor-3 is an inhibitor of KRAS inhibitor. KRAS inhibitor-3 binds to WT and oncogenic KRAS mutants with high affinity (KD: 0.28 μM for KRAS WT, 0.63 μM for KRAS G12C, 0.37 μM for KRAS G12D, 0.74 μM for KRAS Q61H). KRAS inhibitor-3 also disrupts interaction of KRAS with Raf .
1
1 Cited Publications
Cat. No.: HY-18604
CAS No.: 1629265-17-3
K-Ras G12C-IN-1 is an irreversible covalent KRAS G12C inhibitor. K-Ras G12C-IN-1 contains an electrophilic group that forms an irreversible covalent bond with Cys12 of mutant K-Ras. After covalent binding to Cys12, it locks Switch II in an inactive state and interferes with downstream Ras signaling. K-Ras G12C-IN-1 can be used in research related to pancreatic cancer, colon cancer, MYH-associated polyposis, colorectal cancer, and lung cancer .
Synonyms: HL-085
Tunlametinib is a highly selective, orally active MEK1/2 inhibitor (IC50=1.9 nM, MEK1). Tunlametinib blocks the RAS-RAF-MEK-ERK signaling pathway, arrests tumor cell cycle and promotes apoptosis. Tunlametinib potently inhibits the proliferation of RAS/RAF mutant cancer cells (such as BRAF V600E, KRAS G12C mutant cells). Tunlametinib shows synergistic anti-tumor effects with BRAF/KRASG12C/SHP2 inhibitors, Docetaxel (HY-B0011). Tunlametinib can be used to study targeted therapy for RAS/RAF mutation-driven malignancies (such as melanoma, colorectal cancer, and non-small cell lung cancer) .
BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based agent design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) and binds ten-fold more strongly to active KRASG12D versus KRASwt (740 nM vs 7.5 μM). BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.
ARS-1323-alkyne is a covalent inhibitor probe that covalently binds to the Switch-II pocket (S-IIP) of the KRAS G12C mutant protein. ARS-1323-alkyne visualizes the covalent modification of KRAS G12C and quantitatively measures the binding efficiency of the inhibitor to the target. ARS-1323-alkyne can be used to validate the target occupancy of KRAS G12C inhibitors and the synergistic mechanism of combination therapy .
Cat. No.: HY-160023
CAS No.: 2914919-85-8
Synonyms: D3S-001
Elisrasib (D3S-001) is an orally active and selective inhibitor for KRAS. Elisrasib inhibits the proliferation of KRAS G12C mutant H358 and MIA-PA-CA-2. D3S-001 also inhibits the phosphorylation of cellular ERK1/2. Elisrasib exhibits good metabolic stability in hepatocytes, liver microsomes, plasma and whole blood in various species. D3S-001 exhibits good pharmacokinetic characteristics and antitumor efficacy in mice .
Cat. No.: HY-176786
CAS No.: 3104382-00-2
Research Areas:
MCB-36 is a pan-KRAS PROTAC degrader that recruits VHL, with a Kd value of approximately 1 pM against KRAS, and it does not affect KRAS transcription. MCB-36 continuously degrades various KRAS mutants, inhibits oncogenic KRAS signaling pathways, reduces p-ERK levels, and induces apoptosis, thereby suppressing the growth of KRAS-dependent cancer cells. In vivo, MCB-36 inhibits tumor growth, overcomes resistance to KRAS G12C inhibitors, remodels the tumor immune microenvironment and enhances immune cell infiltration. MCB-36 can be used in research related to colorectal cancer and lung cancer .
Cat. No.: HY-164315
CAS No.: 2649788-46-3
KRAS G12C inhibitor 67 (Example 35) is an orally active KRAS G12C inhibitor. KRAS G12C inhibitor 67 inhibits pERK and active KRas. KRAS G12C inhibitor 67 selectively inhibits the growth of various KRAS G12C mutant tumor cell lines. KRAS G12C inhibitor 67 exhibits anticancer activity against esophageal cancer, bladder cancer, colorectal cancer, lung cancer, and pancreatic cancer .
RMC-4998 is an orally active inhibitor targeting the active or GTP-bound state of the KRAS G12C mutant. RMC-4998 can form a ternary complex with intracellular CYPA and the activated KRAS G12C mutant, with an IC50 value of 28 nM. RMC-4998 can inhibit ERK signaling in KRAS G12C mutant cancer cells and induce apoptosis. RMC-4998 can be used for tumor research .
MRTX849 analog 24 is a KRAS G12C inhibitor with a human IC50 of 140 nM. MRTX849 analog 24 binds to KRAS G12C, forms a covalent interaction, and acts as a click probe to bait the protein target in proteomic studies. MRTX849 analog 24 exhibits cellular activity in cancer cells. MRTX849 analog 24 can be used for the research of kras G12C-mutant cancer .
Cat. No.: HY-U00416
CAS No.: 1698024-73-5
ARS-1323 is a KRAS G12C inhibitor. ARS-1323 specifically binds to the cysteine residue on the mutant K-Ras protein, locks it in the GDP-bound conformation, thereby blocking K-Ras activation and downstream signaling pathways. ARS-1323 can be used to investigate the signal transduction mechanisms and growth characteristics of tumor cells driven by K-Ras G12C .
Cat. No.: HY-178042
CAS No.: 2756257-56-2
SS-3091 is a pan-KRas inhibitor active across KRas G12D, KRas G12C, KRas G12V, KRas G12S mutants, with minimal effects on non-KRas-driven cancer cells. SS-3091 binds to the KRas·ARaf interaction interface, destabilizes the complex, and attenuates KRas activity. SS-3091 suppresses phosphorylation of S6K, Akt, and ERK. SS-3091 reduces proliferation and decreases colony formation of cancer cells bearing KRas G12 mutations. SS-3091 can be used for the research of KRas-driven cancers .
Cat. No.: HY-156671A
Purity: 99.02%
RMC-4998 formic is an orally active inhibitor targeting the active or GTP-bound state of the KRAS G12C mutant. RMC-4998 formic can form a ternary complex with intracellular CYPA and the activated KRAS G12C mutant, with an IC50 value of 28 nM. RMC-4998 formic can inhibit ERK signaling in KRAS G12C mutant cancer cells and induce apoptosis. RMC-4998 formic can be used for non-small cell lung cancer (NSCLC) research .
Cat. No.: HY-179403
CAS No.: 2966924-23-0
KRASG12C IN-17 is an orally active covalent KRAS G12C inhibitor, showing strong inhibitory activity in KRAS G12C-mutant cancer cells (NCI-H23 IC50 = 0.7 nM; NCI-H358 IC50 = 0.5 nM).
KRASG12C IN-17 covalently and irreversibly binds to KRAS G12C with > 96% modification efficiency in both GDP-bound and GMPPNP-bound conformations.
KRASG12C IN-17 can be used for studies of KRAS-driven cancers, including colorectal cancer .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
