From 11:00 pm to 12:00 pm EST ( 8:00 pm to 9:00 pm PST ) on January 6th, the website will be under maintenance. We are sorry for the inconvenience. Please arrange your schedule properly.
KRAS inhibitor-41 is an inhibitor of KRAS with IC50 values of <0.01 μM for KRAS G12D and KRASG12V. KRAS inhibitor-41 inhibits RAS mutant cell lines, GP2D (KRAS-G12D) and SW620 (KRAS-G12V). KRAS inhibitor-41 can be used in cancer research .
KRAS inhibitor-31 (compound 33) is a KRAS inhibitor, with KD (SPR) values of 0.019 nM, 0.019 nM and 0.096 nM for KRas G12D, KRas G12C and KRasG12V, respectively .
KRAS inhibitor-37 (compound 2) is a potent KRAS inhibitor with KDs of 0.004 nM, 0.041 nM, 0.019 nM and 0.144 nM for KRAS wild type, KRAS G12D, KRAS G12C and KRASG12V by SPR binding assay, respectively. KRAS inhibitor-37 inhibits cell proliferation with IC50s of <2 nM-14 nM for H358, SW620, PANC08.13 cells, respectively. KRAS inhibitor-37 has the potential for cancer research .
AMG410 is a non-covalent and selective pan-KRAS inhibitor with IC50 values of 1-4 nM for KRAS G12D, KRASG12V, and KRAS G13D. AMG410 shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 is a dual GTP(on)- and GDP(off)-state inhibitor (Kd(GDP-state) of 1 nM; Kd(GTP-state) of 22 nM). AMG410 blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 can be used for the study of colorectal, pancreatic, and lung cancers .
pan-KRAS degrader 1 (Compound 1) is a panKRAS degrader with a surface plasmon resonance (SPR) dissociation constant Ki value of 25 nM for KRASG12V .pan-KRAS degrader 1 has antitumor activity .
pan-KRAS-IN-8 (Compound 38) is an inhibitor for in human tumor mutated genes KRAS, which inhibits proliferation of KRAS mutated cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with IC50 of 0.07 and 0.18 nM, respectively .
pan-KRAS-IN-7 (Compound 25) is an inhibitor for in human tumor mutated genes KRAS, which inhibits proliferation of KRAS mutated cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with IC50 of 0.35 and 0.51 nM, respectively .
pan-KRAS-IN-9 (Compound 52) is an inhibitor for in human tumor mutated genes KRAS, which inhibits proliferation of KRAS mutated cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with IC50 of 0.24 and 0.30 nM, respectively .
pan-KRAS-IN-10 (Compound 58) is an inhibitor for in human tumor mutated genes KRAS, which inhibits proliferation of KRAS mutated cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with IC50 of 0.7 and 0.24 nM, respectively .
pan-KRAS-IN-2 (compound 6) is a pan inhibitor of with IC50s ≤10 nM for KRAS WT and mutants (G12D, G12C, G12V, G12S, G12A, Q61H), and ＞10 μM for KRAS G13D, respectively .
RMC-5127 is an orally active and brain-penetrant mutant-selective tri-complex RAS G12V inhibitor. RMC-5127 non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages RASG12V(ON) to form a high-affinity tri-complex, sterically inhibiting RAS binding . RMC-5127 inhibits the RAS pathway in KRASG12V mutant cancer cells, reducing cell proliferation and inducing apoptosis. RMC-5127 is promising for research of cancers with RAS mutations, such as non-small cell lung cancer .
PROTAC K-Ras degrader-2 (compound 48) is a pan-KRAS-mutant PROTAC degrader with an IC50 of ≤200 nM for KRASG12V/RAF1. PROTAC K-Ras degrader-2 degrades SW620 KRAS G12D with a DC50 of ≤200 nM. PROTAC K-Ras degrader-2 inhibits cell growth of SW620 3D cell with an IC50 of ≤20 nM. (Pink: KRAS inhibitor-30 (HY-164366)) .
KRAS inhibitor-27 (Compound 15h) is the inhibitor for KRAS. KRAS inhibitor-27 inhibits KRAS G12D/G12V mutated cells AsPC-1, SW620 and KRAS wildtype cell HT-29 with IC50 of 378, 0.6 and 3230 nM, respectively. KRAS inhibitor-27 inhibits ERK phosphorylation (IC50 in cell AsPC-1 and SW620 is 0.6 nM and 1 nM), reduces the expression of DUSP4, thereby inhibiting MAPK signaling pathway .
PROTAC K-Ras Degrader-4 (Compound 4) is a PROTAC degrader for KRAS that degrades KRASG12D in GP5d and degrades KRASG12V in cell SW620 with DC50s of 1 nM and 13 nM. PROTAC K-Ras Degrader-4 inhibits MAPK signaling pathway . (Pink: ligand for target protein pan-KRAS degrader 1 (HY-162960); Black: linker (HY-159790); Blue: ligand for E3 ligase VHL (HY-W998248))
SAH-SOS1A is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM), directly and independently blocks nucleotide association, impairs KRAS-driven cancer cell viability, and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
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 KRASG12C cancer models, and demonstrates good tolerability across various RAS cancer models .
PROTAC pan-KRAS degrader-1 is a pan-KRASPROTAC degrader for degrading different KRAS mutation types, such as G12D, G12C, G12V, and G13D. PROTAC pan-KRAS degrader-1 potently degrades KRAS mutation (G12D) in AGS cells, with a DC50 of 1.1 nM, Dmax of 95%. PROTAC pan-KRAS degrader-1 can be used to search diseases caused by KRAS mutation or amplification, especially cancers such as breast cancer, bladder cancer, gastric cancer, etc . Pink: pan-KRAS ligand (HY-176490); Blue: VHL ligase ligand (HY-170353); Black: linker (HY-176491);
SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM). SAH-SOS1A TFA directly and independently blocks nucleotide association. SAH-SOS1A TFA impairs KRAS-driven cancer cell viability and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
RAS inhibitor Abd-7, a potent RAS-binding compound (Kd=51 nM), is a RAS-effector protein-protein interaction (PPI) inhibitor. RAS inhibitor Abd-7 interacts with RAS inside the cells, prevents RAS-effector interactions and inhibits endogenous RAS-dependent signaling. RAS inhibitor Abd-7 impairs the PPI of various mutant KRAS proteins with PI3K, CRAF and RALGDS as well as NRAS Q61H and HRAS G12V .
Pan-RAS-IN-6 (compound 24) is an inhibitor targeting DUSP6, which reduces MAPK activation in the brain of the NCI-H1373-Luc model (DUSP6), at the same time, it shows significant tumor growth inhibition and tumor regression effects in the NSCLC brain metastasis mouse model. Pan-RAS-IN-6 shows high selectivity and strong inhibitory effects, especially in KRAS mutation-related signaling pathways, demonstrating varying inhibitory activity against different KRAS mutants and interacting proteins. The IC50 values for KRAS G12C, G12D, and G12V are 1.3 nM, 4.7 nM, and 0.3 nM, respectively .
Basroparib (STP1002) is a selective, orally active inhibitor of tankyrase (TNKS1/TNKS2) with IC50 of 29.94 nM and 3.68 nM for TNKS1 and TNKS2, respectively. Basroparib has an IC50 of >10 μM for PARP1. Basroparib binds to TNKS, stabilizes AXIN1/2 proteins, blocks Wnt/β-catenin signaling pathway, inhibits tumor cell proliferation and induces apoptosis, while reducing cancer stem cell properties. Basroparib can be used in colorectal cancer (CRC) studies with KRAS mutations (such as G12V/G12D) to overcome acquired resistance to MEK inhibitors. STP1002 has synergistic antitumor activity with MEK inhibitors .
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 (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 (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 .
SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM). SAH-SOS1A TFA directly and independently blocks nucleotide association. SAH-SOS1A TFA impairs KRAS-driven cancer cell viability and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
SAH-SOS1A is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM), directly and independently blocks nucleotide association, impairs KRAS-driven cancer cell viability, and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS .
The Kras4B protein interacts specifically with GPR31, dependent on farnesylation. This binding suggests a regulatory role for Kras4B in association with GPR31, emphasizing the importance of the farnesylation process. Comprehensive exploration into the molecular details of this interaction is crucial to understand the precise mechanisms and functional implications in cellular processes or signaling pathways. Kras4B Protein, Human (G12V, His) is the recombinant human-derived Kras4B protein, expressed by E. coli , with N-6*His labeled tag.
KRAS protein is a key Ras family member that binds GDP/GTP and has intrinsic GTPase activity. Its critical role in regulating cell proliferation emphasizes its importance in cellular processes. KRAS Protein, Human (G12V, His) is the recombinant human-derived KRAS protein, expressed by E. coli , with N-6*His labeled tag and G12V mutation.
HLA-A*1101as is a key MHCI molecule that presents viral and tumor-derived peptides that direct T cell immune responses against infected or transformed cells. It collaborates with B2M to showcase a diverse peptide library. HLA-A*1101 KRAS G12V Complex Protein, Human (HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*1101 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*1101 KRAS G12V Complex Protein, Human (HEK293, His-Avi), has molecular weight of 42-46 kDa.
HLA-A*0301 collaborates with B2M to present viral and tumor peptides that direct CD8-positive T cells to respond against infected or transformed cells. It can also present self-peptides to avoid self-reaction. HLA-A*0301 KRAS G12V Complex Protein, Human (HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*0301 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*0301 KRAS G12V Complex Protein, Human (HEK293, His-Avi), has molecular weight of 55-60 kDa.
HLA-A*0301 collaborates with B2M to present viral and tumor peptides that direct CD8-positive T cells to respond against infected or transformed cells. It can also present self-peptides to avoid self-reaction. HLA-A*0301 KRAS G12V Complex Tetramer Protein, Human (HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*0301 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*0301 KRAS G12V Complex Tetramer Protein, Human (HEK293, His-Avi), has molecular weight of 260-265 kDa.
HLA-A*1101as is a key MHCI molecule that presents viral and tumor-derived peptides that direct T cell immune responses against infected or transformed cells. It collaborates with B2M to showcase a diverse peptide library. HLA-A*1101 KRAS G12V Complex Protein, Human (Biotinylated, VVGAVGVGK, HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*1101 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*1101 KRAS G12V Complex Protein, Human (Biotinylated, VVGAVGVGK, HEK293, His-Avi), has molecular weight of 51-60 kDa.
HLA-A*1101as is a key MHCI molecule that presents viral and tumor-derived peptides that direct T cell immune responses against infected or transformed cells. It collaborates with B2M to showcase a diverse peptide library. HLA-A*1101 KRAS G12V Complex Tetramer Protein, Human (HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*1101 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*1101 KRAS G12V Complex Tetramer Protein, Human (HEK293, His-Avi), has molecular weight of 260-265 kDa.
HLA-A*0301 collaborates with B2M to present viral and tumor peptides that direct CD8-positive T cells to respond against infected or transformed cells. It can also present self-peptides to avoid self-reaction. HLA-A*0301 KRAS G12V Complex Protein, Human (Biotinylated, VVGAVGVGK, HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*0301 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*0301 KRAS G12V Complex Protein, Human (Biotinylated, VVGAVGVGK, HEK293, His-Avi), has molecular weight of 52-60 kDa.
HLA-A*1101as is a key MHCI molecule that presents viral and tumor-derived peptides that direct T cell immune responses against infected or transformed cells. It collaborates with B2M to showcase a diverse peptide library. HLA-A*0301 KRAS G12V Complex Protein, Human (VVGAVGVGK, HEK293, His-Avi) is a recombinant protein dimer complex containing HLA-A*1101 and B2M/Beta-2-microglobulin Protein, expressed by HEK293 , with C-Avi, C-His labeled tag and VVGAVGVGK peptide. HLA-A*0301 KRAS G12V Complex Protein, Human (VVGAVGVGK, HEK293, His-Avi), has molecular weight of 56-65 kDa.
KRAS inhibitor-31 (compound 33) is a KRAS inhibitor, with KD (SPR) values of 0.019 nM, 0.019 nM and 0.096 nM for KRas G12D, KRas G12C and KRasG12V, respectively .
