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Pathways Recommended:	Stem Cell/Wnt Cell Cycle/DNA Damage

Results for "

KRAS G12C-mutant cancer cells

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (1) Apoptosis (5) ERK (4) Galectin (1) MEK (1) Mitochondrial Metabolism (1) mTOR (3) PERK (2) PI3K (3) Ras (9) Reactive Oxygen Species (ROS) (2) Tim3 (1)
By Research Areas:	Cancer (13)
Click Chemistry:	Alkynes (1)

Inhibitors & Agonists

Screening Libraries

Inhibitory Antibodies

Click Chemistry

Targets Recommended: Nuclear Factor of activated T Cells (NFAT) BCRP TREM receptor

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-132844

Tunlametinib HL-085	MEK	Cancer
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) .

HY-156671

RMC-4998	Ras PI3K ERK mTOR Apoptosis	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 .

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 .

HY-156671A

RMC-4998 formic	Ras PI3K ERK mTOR Apoptosis	Cancer
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 .

HY-179403

KRASG12C IN-17	Ras	Cancer
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 .

HY-156671B

RMC-4998 TFA	Ras PI3K ERK mTOR Apoptosis	Cancer
RMC-4998 TFA is an orally active inhibitor targeting the active or GTP-bound state of the KRAS ^G12C mutant. RMC-4998 TFA can form a ternary complex with intracellular CYPA and the activated KRAS ^G12C mutant, with an IC₅₀ value of 28 nM. RMC-4998 TFA can inhibit ERK signaling in KRAS ^G12C mutant cancer cells and induce apoptosis. RMC-4998 TFA can be used for for non-small cell lung cancer (NSCLC) research .

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 .

HY-174851

KRAS G12C-IN-70	Ras	Cancer
KRAS G12C-IN-70 is a selective **KRAS G12C mutant** inhibitor. KRAS G12C-IN-70 blocks KRAS G12C-mediated downstream signaling pathways (e.g., RAF-MEK-ERK) and inhibits tumor cell proliferation. KRAS G12C-IN-70 is promising for research of KRAS G12C mutation-related tumors (such as non-small cell lung cancer, colorectal cancer) .

HY-164389

SML-10-70-1	Ras	Cancer
SML-10-70-1 is a ligand for RAS, which covalently modifies the K-Ras G12C mutant protein, and inhibits the phosphorylation of ERK and Akt. SML-10-70-1 inhibits the proliferation of cancer cells H23, H358 and A549 with IC₅₀ of 26.6-47.6 μM .

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 .

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 .

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 .

HY-179702

KD36	Ras PERK Akt Reactive Oxygen Species (ROS) Apoptosis Mitochondrial Metabolism	Cancer
KD36 is a selective *KRAS-G12C* inhibitor with an IC₅₀ value of 0.92 μM. KD36 can inhibit the phosphorylation of ERK and AKT, induce the accumulation of reactive oxygen species (ROS), reduce mitochondrial membrane potential, thereby leading to apoptosis of KRAS-G12C mutant cells. KD36 can be used in the research of non-small cell lung cancer (NSCLC) .

Cat. No.	Product Name

HY-L260

KRAS Targeted Compound Library	32 compounds
KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) is one of the most important oncogenic driver genes in oncology, with high mutation frequencies in pancreatic cancer, non‑small cell lung cancer, and colorectal cancer. For a long time, KRAS was considered "undruggable" due to the lack of suitable small‑molecule binding pockets on its protein surface. In recent years, with the discovery of the switch‑II pocket and the successful approval of KRAS G12C inhibitors, KRAS‑targeted research has achieved groundbreaking progress, which has also spurred a wave of development targeting non‑G12C mutants such as G12D and G12V, as well as upstream and downstream regulatory factors including SOS1 and SHP2. MCE KRAS Targeted Compound Library contains 32 small‑molecule compounds targeting the KRAS, serving as high‑quality research tools for mechanistic studies of KRAS‑mutant tumors, combination therapy development, resistance mechanism exploration, and high‑throughput drug screening, thereby providing robust support for KRAS‑targeted drug discovery.

KRAS Targeted Compound Library

32 compounds

KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) is one of the most important oncogenic driver genes in oncology, with high mutation frequencies in pancreatic cancer, non‑small cell lung cancer, and colorectal cancer. For a long time, KRAS was considered "undruggable" due to the lack of suitable small‑molecule binding pockets on its protein surface. In recent years, with the discovery of the switch‑II pocket and the successful approval of KRAS G12C inhibitors, KRAS‑targeted research has achieved groundbreaking progress, which has also spurred a wave of development targeting non‑G12C mutants such as G12D and G12V, as well as upstream and downstream regulatory factors including SOS1 and SHP2.

MCE KRAS Targeted Compound Library contains 32 small‑molecule compounds targeting the KRAS, serving as high‑quality research tools for mechanistic studies of KRAS‑mutant tumors, combination therapy development, resistance mechanism exploration, and high‑throughput drug screening, thereby providing robust support for KRAS‑targeted drug discovery.

Cat. No.	Product Name	Target	Research Area	Image

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 .

Cat. No.	Product Name		Classification

HY-179403

KRASG12C IN-17		Alkynes
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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BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.

BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

MedchemExpress Validation 03

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred

MedchemExpress Validation 04

MedchemExpress Validation

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