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oncogenic KRAS

" in MedChemExpress (MCE) Product Catalog:

31

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7

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3

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-148439
    Daraxonrasib
    Maximum Cited Publications
    10 Publications Verification

    RMC-6236; RAS-IN-2

    		 Ras PERK Cancer
    Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS (ON) inhibitor. Daraxonrasib disrupts the interaction of wild-type or mutant RAS proteins with the RAS binding domain of BRAF, with EC50 values ranging from 28-220 nM for wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. Daraxonrasib inhibits pERK. Daraxonrasib has anti-tumor activity against KRAS mutant tumors .
    Daraxonrasib
  • HY-145928
    Divarasib
    5+ Cited Publications

    GDC-6036

    		 Ras Cancer
    Divarasib (GDC-6036) is an orally active, selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds Cys12 in GDP-bound KRAS G12C, occupies the switch II pocket, blocks GTP binding and SOS-mediated reactivation, and inhibits oncogenic KRAS signaling. Divarasib induces tumor shrinkage and robust tumor growth inhibition in KRAS G12C-positive models and cancer cells. Divarasib can be used for the research of non-small cell lung cancer, colorectal adenocarcinoma, pancreatic ductal adenocarcinoma, and other KRAS G12C-mutated solid tumors .
    Divarasib
  • HY-157228
    ACBI3

    		PROTACs Ras Cancer
    ACBI3 (compound 7), a chemical probe, is a PROTAC targeting KRAS. ACBI3 is composed of PROTAC target protein ligand pan-KRAS degrader 1 (HY-162960) (red part), E3 ligase ligand E3 ligase Ligand 43 (HY-401613) (blue part) and PROTAC Linker 1-Bromo-4-(ethynyloxy)butane (HY-169992) (black part), among which the conjugate of E3 ubiquitin ligase ligand + Linker is E3 Ligase Ligand-linker Conjugate 143 (HY-169995). ACBI3 achieves in vivo degradation of oncogenic KRAS, resulting in durable pathway modulation and tumor regressions in KRAS mutant xenograft mouse models .
    ACBI3
  • HY-15872A
    FTI-277 hydrochloride
    5+ Cited Publications

    		 Farnesyl Transferase Apoptosis Ras Infection Cancer
    FTI-277 hydrochloride is an inhibitor of farnesyl transferase (FTase); a highly potent Ras CAAX peptidomimetic which antagonizes both H- and K-Ras oncogenic signaling. FTI-277 hydrochloride can inhibit hepatitis delta virus (HDV) infection.
    FTI-277 hydrochloride
  • HY-176786
    MCB-36

    		PROTACs Ras Apoptosis PERK p38 MAPK Caspase TNF Receptor Cancer
    MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities Kd ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .
    MCB-36
  • HY-B0984
    Fendiline hydrochloride
    3 Publications Verification

    		 Calcium Channel Ras STING Autophagy Infection Cardiovascular Disease Cancer
    Fendiline hydrochloride, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline hydrochloride is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline hydrochloride inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline hydrochloride is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10) .
    Fendiline hydrochloride
  • HY-B0984A
    Fendiline
    3 Publications Verification

    		 Calcium Channel Ras STING Autophagy Infection Cardiovascular Disease Cancer
    Fendiline, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10) .
    Fendiline
  • HY-176785S
    MCB-294

    		Ras Apoptosis p38 MAPK Caspase TNF Receptor Cancer
    MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with Kds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC50s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .
    MCB-294
  • HY-122914
    KRAS inhibitor-3
    1 Publications Verification

    		 Ras Cancer
    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 .
    KRAS inhibitor-3
  • HY-151523
    KRas G12R inhibitor 1

    		Ras Cancer
    KRas G12R inhibitor 1 is a covalent inhibitor targeting the common oncogenic mutant KRas G12R with selectivity for the mutant arginine. KRas G12R inhibitor 1 possesses an α,β-diketoamide and exploits strong nucleophilicity of the mutant cysteine and irreversibly binds in the Switch II region of KRas. KRas G12R inhibitor 1 can be researched for K-Ras (G12R)-driven cancer such as pancreatic ductal adenocarcinoma (PDAC) .
    KRas G12R inhibitor 1
  • HY-139402
    MRTX849 acid

    		Ras Cancer
    MRTX849 acid, a derivative of MRTX849, can be used in the synthesis of PROTAC LC-2 (HY-137516). LC-2 is a potent and first-in-class PROTAC capable of degrading endogenous KRAS G12C (DC50s between 0.25 and 0.76 μM) .
    MRTX849 acid
  • HY-B0984R
    Fendiline hydrochloride (Standard)

    		Calcium Channel Ras STING Autophagy Reference Standards Infection Cardiovascular Disease Cancer
    Fendiline (hydrochloride) (Standard) is the analytical standard of Fendiline (hydrochloride). This product is intended for research and analytical applications. Fendiline hydrochloride, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC50 of 17 µM). Fendiline hydrochloride is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline hydrochloride inhibits K-Ras plasma membrane localization (IC50 of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline hydrochloride is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10) .
    Fendiline hydrochloride (Standard)
  • HY-115489
    GGTI-286

    		Ras Cancer
    GGTI-286, a potent and cell-permeable GGTase I inhibitor, is 25-fold more potent (IC50=2 μM) than the corresponding methyl ester of FTI-276 (HY-15873A). GGTI-286 selectively inhibits geranylgeranylation of Rap1A over farnesylation of H-Ras in NIH3T3 cells (IC50s=2 and >30 μM, respectively). GGTI-286 also potently inhibits oncogenic K-Ras4B stimulation with an IC50 of 1 μM .
    GGTI-286
  • HY-115489A
    GGTI-286 TFA

    		Protein Prenyltransferase Cancer
    GGTI-286 TFA, a potent and cell-permeable GGTase I inhibitor, is 25-fold more potent (IC50=2 μM) than the corresponding methyl ester of FTI-276 (HY-15873A). GGTI-286 TFA selectively inhibits geranylgeranylation of Rap1A over farnesylation of H-Ras in NIH3T3 cells (IC50s=2 and >30 μM, respectively). GGTI-286 TFA also potently inhibits oncogenic K-Ras4B stimulation with an IC50 of 1 μM .
    GGTI-286 TFA
  • HY-145928B
    Divarasib adipate
    5+ Cited Publications

    GDC-6036 adipate

    		 Ras Cancer
    Divarasib (GDC-6036) adipate is an orally active, selective KRASG12C inhibitor with an IC50 of <0.01 μM. Divarasib adipate covalently binds Cys12 in GDP-bound KRASG12C, occupies the switch II pocket, blocks GTP binding and SOS-mediated reactivation, and inhibits oncogenic KRAS signaling. Divarasib adipate induces tumor shrinkage and robust tumor growth inhibition in KRASG12C-positive models and cancer cells. Divarasib adipate can be used for the research of non-small cell lung cancer, colorectal adenocarcinoma, pancreatic ductal adenocarcinoma, and other KRASG12C-mutated solid tumors .
    Divarasib adipate
  • HY-108436
    Deltazinone 1

    		Phosphodiesterase (PDE) Cancer
    Deltazinone 1, a pyrazolopyridazinone, is a highly selective PDEδ inhibitor with a KD of 8 nM. Deltazinone 1 inhibits the PDEδ-Ras interaction. Deltazinone 1 shows a dose-dependent inhibitory response on proliferation in oncogenic KRas-dependent cell lines .
    Deltazinone 1
  • HY-P10436
    Braftide

    		Raf Cancer
    Braftide is an allosteric inhibitor for BRAF kinase by targeting the dimer interface of BRAF kinase and inhibiting the formation of BRAF dimers. Braftide inhibits wild-type BRAF and oncogenic BRAF G469A with IC50 of 364 nM and 172 nM, respectively. Braftide inhibits MAPK signaling pathway, inhibits proliferation of KRAS mutant tumor cells (EC50 is 7.1 and 6.6 μM, for HCT116 and HCT-15), in combination of TAT sequence. Braftide can be used for cancer research .
    Braftide
  • HY-P11355A
    KRAS WT Peptide TFA

    		Amino Acid Derivatives Cancer
    KRAS WT Peptide TFA is the trifluoroacetate salt of KRAS WT Peptide (HY-P11355). KRAS WT Peptide is the normal sequence peptide of the Kirsten rat sarcoma virus (KRAS) gene without oncogenic mutations. KRAS WT Peptide can be used for the study of evaluating the specificity and safety of KRAS-targeted immunotherapies .
    KRAS WT Peptide TFA
  • HY-P11356
    KRAS G12V Peptide

    		IFNAR Cancer
    KRAS G12V Peptide is a specific peptide derived from the Kirsten rat sarcoma virus (KRAS) gene carrying the G12V oncogenic mutation. KRAS G12V Peptide induces responses like IFN-γ secretion and cytotoxicity. KRAS G12V Peptide can be used for the study of immune responses against KRAS G12V-mutant tumors .
    KRAS G12V Peptide
  • HY-P11357A
    KRAS G12C Peptide TFA

    		IFNAR Cancer
    KRAS G12C Peptide TFA is the trifluoroacetate salt of KRAS G12C Peptide (HY-P11357). KRAS G12C Peptide is a specific peptide derived from the Kirsten rat sarcoma virus (KRAS) gene carrying the G12C oncogenic mutation. KRAS G12C Peptide induces responses like IFN-γ secretion and cytotoxicity. KRAS G12C Peptide can be used for the study of immune responses against KRAS G12C-mutant tumors .
    KRAS G12C Peptide TFA
  • HY-P11356A
    KRAS G12V Peptide TFA

    		IFNAR Cancer
    KRAS G12V Peptide TFA is the trifluoroacetate salt of KRAS G12V Peptide (HY-P11355). KRAS G12V Peptide is a specific peptide derived from the Kirsten rat sarcoma virus (KRAS) gene carrying the G12V oncogenic mutation. KRAS G12V Peptide induces responses like IFN-γ secretion and cytotoxicity. KRAS G12V Peptide can be used for the study of immune responses against KRAS G12V-mutant tumors .
    KRAS G12V Peptide TFA
  • HY-116428
    L-744832

    		Farnesyl Transferase Ras TGF-β Receptor Apoptosis Cancer
    L-744832 is a farnesyl transferase inhibitor. L-744832 effectively inhibits the farnesylation of H-Ras and N-Ras, but has little effect on K-Ras treatment. L-744832 not only directly targets the oncogenic pathway by inhibiting Ras farnesylation, but also enhances radiosensitivity by restoring TGF-β signaling through epigenetic reprogramming. L-744832 can induce cell cycle arrest and apoptosis. L-744832 can be used in combination therapy studies for Ras-driven tumors such as pancreatic cancer .
    L-744832
  • HY-P11357
    KRAS G12C Peptide

    		IFNAR Cancer
    KRAS G12C Peptide is a specific peptide derived from the Kirsten rat sarcoma virus (KRAS) gene carrying the G12C oncogenic mutation. KRAS G12C Peptide induces responses like IFN-γ secretion and cytotoxicity. KRAS G12C Peptide can be used for the study of immune responses against KRAS G12C-mutant tumors .
    KRAS G12C Peptide
  • HY-151287
    KRAS inhibitor-20

    		Ras Cancer
    KRAS inhibitor-20 is a small molecular inhibitor of KRas G12C, the oncogenic mutant. KRAS inhibitor-20 inhibits KRas G12C with the IC50 value <10 nM .
    KRAS inhibitor-20
  • HY-120885
    (+)-Oxanthromicin

    		Ras Cancer
    (+)-Oxanthromicin (Compound 1) mislocalizes the oncogenic mutant K-Ras from the plasma membrane of intact Madin-Darby canine kidney (MDCK) cells, and exhibits thereby antitumor efficacy .
    (+)-Oxanthromicin
  • HY-137971
    (±)-Spiro-oxanthromicin A

    		Ras Cancer
    (±)-Spiro-oxanthromicin A (Compound 4), a polyketide, is a K-Ras inhibitor with an IC50 of 26.7  μM. (±)-Spiro-oxanthromicin A can be isolated from soil-derived Streptomyces sp. (±)-Spiro-oxanthromicin A can mislocalize oncogenic mutant K-Ras from the plasma membrane of intact MDCK cells. (±)-Spiro-oxanthromicin A can be used for cancers research .
    (±)-Spiro-oxanthromicin A
  • HY-117935
    GGTI-286 hydrochloride

    		Ras Cancer
    GGTI-286 hydrochloride, a potent GGTase I inhibitor, is 25-fold more potent (IC50=2 μM) than the corresponding methyl ester of FTI-276 (HY-15873A). GGTI-286 hydrochloride selectively inhibits geranylgeranylation of Rap1A over farnesylation of H-Ras in NIH3T3 cells (IC50s =2 and >30 μM, respectively). GGTI-286 hydrochloride also potently inhibits oncogenic K-Ras4B stimulation with an IC50 of 1 μM .
    GGTI-286 hydrochloride
  • HY-183625
    PCA-IN-1

    		Ras Cancer
    PCA-IN-1 is a polyisoprenylated cysteinyl amide (PCA) inhibitor that acts on multiple KRAS mutant subtypes. PCA-IN-1 dissociates KRAS4B from its transport chaperones, prevents its localization to the plasma membrane, and blocks downstream oncogenic signaling pathways. PCA-IN-1 inhibits colony formation of KRAS-mutant lung cancer cells, induces sustained long-term growth inhibition, and suppresses cell migration. PCA-IN-1 is applicable to the research of KRAS-mutant lung cancer .
    PCA-IN-1
  • HY-181883
    KRAS-IN-55

    		Ras Raf PI3K p38 MAPK Cancer
    KRAS-IN-55 is a pan-KRAS inhibitor with IC50 values of 4.3, 9.6 and 1.6 nM against KRAS G12C, KRAS G12D and KRAS G12V, respectively. KRAS-IN-55 induces the formation of a new binding pocket on KRAS, thereby forming a high-affinity ternary complex with cyclophilin A (CYPA), inhibiting the interactions of KRAS with downstream effectors RAF and PI3K, and blocking oncogenic MAPK and PI3K signaling pathways. KRAS-IN-55 is applicable to cancer research such as colorectal cancer and non-small cell lung cancer .
    KRAS-IN-55
  • HY-182883
    KRASG12C IN-20

    		Ras Cancer
    KRASG12C IN-20 is an orally potent KRAS G12C inhibitor with an EC50 of 3.9 nM. KRASG12C IN-20 covalently modifies KRAS G12C in its inactive GDP-bound state and locks it to block oncogenic signal transduction. KRASG12C IN-20 exhibits significant activity in lung adenocarcinoma xenograft models. KRASG12C IN-20 can be used for research related to lung adenocarcinoma .
    KRASG12C IN-20
  • HY-134505
    Avicin G

    		Ras Phospholipase ERK Akt Cancer
    Avicin G is a sphingomyelinase inhibitor and plasma membrane disruptor. Avicin G inhibits the enzymatic activities of neutral sphingomyelinases (SMPD2/3) and acid sphingomyelinase (SMPD1), elevates intracellular sphingomyelin levels, and alters the distribution of sphingomyelin. Avicin G interferes with the lateral segregation of GTP- and GDP-bound H-Ras, inhibits the signal output of oncogenic K-Ras and H-Ras, reduces the phosphorylation of ERK and Akt, increases lysosomal pH, and inhibits the endocytic recycling of epidermal growth factor receptor. Avicin G can be used in research related to pancreatic ductal adenocarcinoma and non-small cell lung cancer .
    Avicin G

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