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Results for "

KRAS mutant pancreatic cancer

" in MedChemExpress (MCE) Product Catalog:

33

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Targets Recommended:
Cat. No. 상품명 Target 연구분야 Chemical Structure
  • HY-173629
    RMC-5127

    		Ras Apoptosis Cancer
    RMC-5127 is a small molecule inhibitor that binds to GTP-targeted KRAS G12V, with oral bioavailability and blood-brain barrier permeability. RMC-5127 inhibits the activities of the RAS and MAPK pathways, suppresses the proliferation of KRAS G12V-mutant cancer cells and induces their apoptosis. RMC-5127 can be used for the research of KRAS G12V-mutant non-small cell lung cancer, pancreatic ductal adenocarcinoma, colorectal cancer and intracranial KRAS G12V tumors .
    RMC-5127
  • HY-176523
    KRAS G12D-IN-29

    		Ras Cancer
    KRAS G12D inhibitor 29 (Compound Formula (I)) is an orally active and selective KRAS G12D mutant inhibitor. KRAS G12D inhibitor 29 blocks downstream signaling pathways mediated by KRAS G12D, suppressing tumor cell proliferation. KRAS G12D inhibitor 29 is promising for research of KRAS G12D mutation-related cancers (such as pancreatic cancer, lung cancer, colorectal cancer) .
    KRAS G12D-IN-29
  • HY-114491
    Rineterkib

    		ERK Raf Cancer
    Rineterkib (compound B) is an orally available ERK1 and ERK2 inhibitor in the treatment of a proliferative disease characterized by activating mutations in the MAPK pathway. The activity is particularly related to the treatment of KRAS-mutant NSCLC, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC) and KRAS-mutant ovarian cancer. Rineterkib hydrochloride can also inhibit RAF .
    Rineterkib
  • HY-164315
    KRAS G12C inhibitor 67

    		Ras PERK Cancer
    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 .
    KRAS G12C inhibitor 67
  • 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-162809
    XMU-MP-9

    		Ras Cancer
    XMU-MP-9 is a bifunctional compound that binds to the C2 domain of Nedd4-1 and the allosteric site of K-Ras. XMU-MP-9 enhances the interaction between Nedd4-1 and K-Ras, induces conformational changes in the Nedd4-1/K-Ras complex, promotes the ubiquitination and degradation of multiple K-Ras mutants, and inhibits the proliferation of cells carrying K-Ras mutants. XMU-MP-9 can be used for the study of colon, lung and pancreatic cancer .
    XMU-MP-9
  • 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-156529
    pan-KRAS-IN-2

    		Ras Cancer
    pan-KRAS-IN-2 (Compound 6) is a pan-inhibitor with IC50s ≤ 10 nM for KRAS WT and mutants (G12D, G12C, G12V, G12S, G12A and Q61H); and an IC50 > 10 μM for KRAS G13D. pan-KRAS-IN-2 can be used to study various KRAS-mediated cancers, such as pancreatic cancer and colorectal cancer .
    pan-KRAS-IN-2
  • 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-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-175025
    CH091138

    		PROTACs Ras Apoptosis Cancer
    CH091138 is a potent and selective KRASG12D PROTAC degrader with DC50s of 148.3 nM in HeLa cells and 469.8 nM in AsPC-1 cells. CH091138 selectively degrades exogenous and endogenous KRASG12D but not KRAS WT or other KRAS mutants (G12C/G12S/G12V), depending on the VHL-mediated ubiquitin-proteasome system. CH091138 exhibits potent anti-tumor activity and induces cancer cell apoptosis. CH091138 can be used for the studies of pancreatic cancer and colon cancer. (Pink: KRASG12D ligand (HY-175144); Blue: VHL E3 ligase ligand (HY-138678); Black: Linker; VHL E3 ligase ligand + Linker (HY-136006B)) .
    CH091138
  • HY-157458
    PDEδ autophagic degrader 1

    		ATTECs Phosphodiesterase (PDE) Autophagy Cancer
    PDEδ autophagic degrader 1 (compound 12c), an autophagosome-tethering compound (ATTEC). is a potent PDEδ autophagic degrader. PDEδ autophagic degrader 1 reduces the PDEδ protein level through lysosome-mediated autophagy without affecting the PDEδ mRNA expression. PDEδ autophagic degrader 1 suppresses the growth in KRAS mutant pancreatic cancer cells .
    PDEδ autophagic degrader 1
  • HY-159591
    YK-8S

    		Ras Akt ERK Cancer
    YK-8S is a dual-targeted K-Ras (G12D/G12C) covalent inhibitor. YK-8S shows no significant binding to wild-type K-Ras and other mutants (G12R, G13D, Q61R/K). YK-8S exhibits anti-proliferative activity against H358 (G12C) and AGS (G12D) cells. YK-8S inhibits the phosphorylation of p-AKT/p-ERK in BaF3/G12D and G12C cells. YK-8S can be used for pancreatic cancer, colorectal cancer and other tumors with high incidence of G12D .
    YK-8S
  • HY-162445
    KRASG12D-IN-3

    		Ras PERK Cancer
    KRASG12D-IN-3 is an orally active KRAS G12D inhibitor. KRASG12D-IN-3 inhibits the growth of gastric cancer and pancreatic cancer cells. KRASG12D-IN-3 inhibits the activity of p-ERK in gastric cancer cells. KRASG12D-IN-3 can be used for the research of gastric cancer and pancreatic cancer .
    KRASG12D-IN-3
  • HY-174261
    KRAS-IN-5

    		Ras Cancer
    KRAS-IN-5 (Compound Ex 6) is an orally active and selective inhibitor targeting KRAS mutants (including KRAS G12D, KRAS G12V, KRAS WT) with a GNE IC50 value of 1.3 nM against KRAS G12D. KRAS-IN-5 blocks tumor cell proliferation by inhibiting KRAS-mediated signaling pathways (e.g., reducing ERK phosphorylation). KRAS-IN-5 is promising for research of KRAS mutation-related cancers, such as pancreatic cancer, colorectal cancer, lung cancer .
    KRAS-IN-5
  • HY-172919
    PDEδ/NAMPT IN-1

    		Phosphodiesterase (PDE) NAMPT Apoptosis Cancer
    PDEδ/NAMPT IN-1 (Compound 17d) is a dual inhibitor targeting phosphodiesterase 6 (PDE6) (KD=0.410 nM) and nicotinamide phosphoribosyl transferase (NAMPT) (IC50=2.21 nM). PDEδ/NAMPT IN-1 blocks KRAS-related signal transduction and interferes with the synthesis of nicotinamide adenine dinucleotide (NAD +), inducing apoptosis in KRAS mutant pancreatic cancer cells. PDEδ/NAMPT IN-1 is promising for research of KRAS mutant pancreatic cancer .
    PDEδ/NAMPT IN-1
  • HY-178497
    ZJK-807

    		PROTACs Ras p38 MAPK TNF Receptor Inflammation/Immunology Cancer
    ZJK-807 is a highly effective and selective PROTAC degrader targeting KRASG12D (DC50 = 79.5 nM in AsPC-1 cells). ZJK-807 shows minimal impact on wild-type KRAS or other mutants (G12C/S/V, G13D), inducing mutant-specific cytotoxicity. ZJK-807 suppresses RAS/MAPK signaling and uniquely modulates TNF signaling and eukaryotic ribosome biogenesis. ZJK-807 can be used for the study of KRAS-driven pancreatic cancer. Yellow: KRASG12D ligand (HY-W087383); Green: E3 ligase CRBN ligand (HY-178507); Black: Linker (HY-178506) .
    ZJK-807
  • HY-154313
    Spiclomazine

    Clospirazine

    		 Ras Cancer
    Spiclomazine (Clospirazine) is a potent mutant KRAS(G12C) inhibitor that selectively inhibits mutant KRAS-driven pancreatic cancer. Spiclomazine can eliminate KRas-GTP levels in KRAS-driven pancreatic cancer and effectively inhibit RAS-mediated signaling. Spiclomazine significantly inhibits tumor progression in mouse renal capsule xenotransplantation models .
    Spiclomazine
  • HY-175144
    KRASG12D-IN-6

    		Ligands for Target Protein for PROTAC Ras Cancer
    KRASG12D-IN-6 is a PROTAC target protein ligand that can be used to synthesize CH091138 (HY-175025). CH091138 is a potent and selective KRASG12D PROTAC degrader with anti-tumor activity .
    KRASG12D-IN-6
  • HY-114491A
    Rineterkib hydrochloride

    		ERK Raf Cancer
    Rineterkib hydrochloride (compound B) is an orally available ERK1 and ERK2 inhibitor in the treatment of a proliferative disease characterized by activating mutations in the MAPK pathway. The activity is particularly related to the treatment of KRAS-mutant NSCLC, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC) and KRAS-mutant ovarian cancer. Rineterkib hydrochloride can also inhibit RAF .
    Rineterkib hydrochloride
  • HY-149607
    SHP2-IN-22

    		SHP2 Cancer
    SHP2-IN-22 is SHP2 allosteric inhibitor with an IC50 value of 17.7 nM. SHP2-IN-22 inhibits the proliferation, migration, and invasion of MIA PaCa-2 pancreatic cancer cells. SHP2-IN-22 can be used for Kirsten rat sarcoma viral oncogene (KRAS) mutant cancer research .
    SHP2-IN-22
  • HY-175326
    SOS1-IN-21

    		SOS1 Cancer
    SOS1-IN-21 is an orally active inhibitor of son of Sevenless 1 (SOS1) with an IC50 of 15 nM. SOS1 is a guanine nucleotide exchange factor (GEF) that activates KRAS by facilitating the exchange of GDP for GTP. SOS1-IN-21 exhibits potent antiproliferative activity, with IC50 values of 16 nM in NCI-H358 and 17 nM in Mia Paca-2 cell proliferation assays. SOS1-IN-21 exhibits significant antitumor activity in the Mia Paca-2 xenograft model. SOS1-IN-21 can be used for the study of KRAS mutant tumors, such as pancreatic cancer .
    SOS1-IN-21
  • HY-P992366
    HFB200901

    		Galectin Tim3 Cancer
    HFB200901 is a galectin LGALS9 inhibitor and immunostimulant that can be used in studies related to pancreatic adenocarcinoma, pancreatic intraepithelial neoplasia, KRAS G12C-mutant colon cancer, and prostate cancer. HFB200901 disrupts the LGALS9/TIM-3 axis, while blocking the internalization and vacuolization of recombinant LGALS9. HFB200901 reduces the proportion of regulatory T cells (Treg) and enhances dendritic cell activation, thereby inducing polyfunctional and memory CD8 + T cell responses. HFB200901 inhibits the progression of pancreatic neoplastic lesions and effectively improves the efficacy of PSMA-based vaccination .
    HFB200901
  • HY-181704
    KRAS-IN-54

    		PERK Ras Cancer
    KRAS-IN-54 is a macrocyclic KRAS inhibitor. KRAS-IN-54 exhibits activity against cell viability and pERK inhibition in cells with KRAS G12D and KRAS G13D mutations. KRAS-IN-54 can be used in the research of KRAS-mutant cancers, including pancreatic adenocarcinoma, colorectal cancer, non-small cell lung cancer, esophageal cancer, gallbladder cancer, melanoma, ovarian cancer and endometrial cancer .
    KRAS-IN-54
  • HY-181716
    KRAS G12C-IN-74

    		Ras Apoptosis Cancer
    KRAS G12C-IN-74 is an orally active, selective KRAS G12C inhibitor with a target IC50 of 43.18 nM. KRAS G12C-IN-74 induces G0/G1 cell cycle arrest and apoptosis in KRAS G12C-mutant cancer cells. KRAS G12C-IN-74 is applicable for the research of KRAS G12C-mutant pancreatic cancer, colorectal cancer and lung cancer .
    KRAS G12C-IN-74
  • HY-180885S
    KRAS G12D-IN-35

    		Ras ERK Cancer
    KRAS G12D-IN-35 (example 7) is a potent and orally active KRAS G12D inhibitor. KRAS G12D-IN-35 suppresses p-ERK in AGS cells and potently inhibits the proliferation of various KRAS G12D-mutant cancer cell lines. KRAS G12D-IN-35 inhibits tumor growth in HPAC and GP2D mouse models. KRAS G12D-IN-35 can be used for cancer research, such as pancreatic and colorectal cancer .
    KRAS G12D-IN-35
  • HY-179484
    KRASG12C IN-19

    		Reactive Oxygen Species (ROS) ERK Cancer
    KRASG12C IN-19 is a selective and orally active KRAS G12C inhibitor. KRASG12C IN-19 exerts potent antiproliferative activity against the KRAS G12C-mutant non small cell lung cancer (NSCLC) cell line H358 with an IC50 of 7.6 nM, and effectively suppresses downstream ERK phosphorylation (IC50 = 24.06 nM). KRASG12C IN 19 has no significant inhibitory activity against KRAS G12V and KRAS G12D-mutant cancer cells (PANC 1, Panc, AsPC 1, and GP2d cells) with IC50 > 10,000 nM. KRASG12C IN-19 rapidly forms a covalent bond with KRAS G12V-GDP, leading to dose-dependent inhibition of the downstream KRAS pathway. KRASG12C IN 19 can be employed for research in KRAS G12C driven cancers, including non small cell lung cancer, pancreatic cancer, and colorectal cancer .
    KRASG12C IN-19
  • HY-181964
    KRAS G12C-IN-77

    		Cancer
    KRAS G12C-IN-77 is an orally active and selective KRAS G12C covalent dual-state inhibitor that binds with high affinity to both GDP-bound (inactive state) and GTP-bound (active state) KRAS G12C (IC50 = 133 nM). KRAS G12C-IN-77 rapidly inhibits ERK1/2 phosphorylation, induces the formation of covalent adducts with endogenous KRAS G12C, suppresses the expression of MAPK pathway genes, and inhibits the proliferation of KRAS G12C-mutant cells. KRAS G12C-IN-77 is applicable to research related to KRAS G12C-mutant solid tumors, including pancreatic ductal adenocarcinoma and non-small cell lung cancer .
    KRAS G12C-IN-77
  • HY-182241
    JR4-187

    		c-Myc Early 2 Factor (E2F) TNF Receptor MDM-2/p53 Reactive Oxygen Species (ROS) Apoptosis Cancer
    JR4-187 is an orally active, copper-dependent anticancer agent. JR4-187 downregulates genes involved in oxidative phosphorylation, MYC targets and E2F targets in cancer cells, while upregulates genes involved in the TNF-α signaling pathway, p53 pathway and KRAS signaling pathway, and downregulates CTR1 protein . JR4-187 induces ROS production, apoptosis, copper-dependent cytotoxicity, and exhibits selective cytotoxicity against KRAS-mutant cancer cells. JR4-187 is well tolerated in mouse models of pancreatic cancer. JR4-187 can be used in research related to cancers such as pancreatic ductal adenocarcinoma, colon cancer and rectal cancer .
    JR4-187
  • HY-181965
    KRAS G12C-IN-78

    		Ras ERK p38 MAPK Cancer
    KRAS G12C-IN-78 is a selective SWII-binding KRASG12C dual inhibitor targeting both inactive and active states. KRAS G12C-IN-78 rapidly inhibits ERK1/2 phosphorylation, induces covalent adduct formation with endogenous KRASG12C, suppresses MAPK pathway gene expression, and inhibits cellular proliferation in KRASG12C mutant cells. KRAS G12C-IN-78 can be used for the research of KRASG12C mutant solid tumors, including pancreatic ductal adenocarcinoma and non-small cell lung cancer .
    KRAS G12C-IN-78
  • HY-175870A
    (7R)-Eras-4001

    		Ras ERK Cancer
    (7R)-Eras-4001 is an orally active KRAS mutant inhibitor with remarkable selectivity for H-RAS and N-RAS. (7R)-Eras-4001 effectively suppresses cancer cell viability by blocking downstream signaling pathways mediated by RAF family proteins, inhibiting the formation of the KRAS G12D-RAF1 RBD complex and the phosphorylation of ERK1/2. (7R)-Eras-4001 induces tumor growth inhibition and regression in a dose-dependent manner, and also reduces plasma ERK1/2 phosphorylation levels. (7R)-Eras-4001 exerts a synergistic effect with anti-PD-1 Cetuximab (HY-P9905). (7R)-Eras-4001 can be used in research on non-small cell lung cancer, pancreatic cancer, colorectal cancer, and ovarian cancer .
    (7R)-Eras-4001
  • HY-180200
    RNK08954

    		Ras ERK Cancer
    RNK08954 is an orally active KRASG12D inhibitor with a Kd of 0.0395 nM. RNK08954 selectively binds the inactive GDP-bound KRASG12D form, suppresses downstream KRAS-mediated signaling pathways p-ERK1/2 experssion. RNK08954 inhibits KRASG12D-mutant cell proliferation, induces G0-G1 cell cycle arrest, and inhibits tumor growth in mouse xenograft models. RNK08954 can be used for the research of non-small cell lung cancer, pancreatic ductal adenocarcinoma .
    RNK08954
  • HY-181913
    KRAS G12C-IN-76

    		Ras ERK Cancer
    KRAS G12C-IN-76 (Compound 39) is an orally active KRAS G12C inhibitor. KRAS G12C-IN-76 inhibits the phosphorylation of ERK. KRAS G12C-IN-76 exhibits anticancer activity against pancreatic cancer .
    KRAS G12C-IN-76

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