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 G12C inhibitor 60 (compound 23) is a Kras-G12C inhibitor. KRAS G12C inhibitor 60 can be used for the research of lung cancer, colorectal cancer, pancreatic cancer .
KRAS G12C inhibitor 65 is a potent and covalent KRAS G12C inhibitor that traps KRAS G12C in the GDP-bound state. KRASG12C IN-1 exhibits potent antitumor activity against KRAS-mutant non-small cell lung cancer .
KRAS G12C inhibitor 29 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 3. KRAS G12C inhibitor 29 can be used for the research of cancer .
KRAS G12C inhibitor 30 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 2. KRAS G12C inhibitor 30 can be used for the research of cancer .
KRAS G12C inhibitor 31 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 1. KRAS G12C inhibitor 31 can be used for the research of cancer .
KRAS G12C inhibitor 33 is a KRAS G12C inhibitor extracted from patent WO2021244603A1, compound 1. KRAS G12C inhibitor 33 can be used for the research of cancer .
KRAS G12C inhibitor 34 is a KRAS G12C inhibitor extracted from patent WO2021239058A1, compound Z1. KRAS G12C inhibitor 34 can be used for the research of cancer .
KRAS G12C inhibitor 62 is a KRAS G12C inhibitor. KRAS G12C inhibitor 62 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2021121367A1) .
KRAS G12C inhibitor 44 (compound 54) is a potent and orally active KRAS G12C inhibitor. KRAS G12C inhibitor 44 shows anti-proliferation activities with IC50s of 0.016, 0.028 µM in MIA PaCA-2, H358 cells, respectively. KRAS G12C inhibitor 44 shows antitumor effects in vivo .
KRAS G12C inhibitor 47 (compound 8-1-1) is a potent KRAS G12C inhibitor with an IC50 of 0.172 µM. KRAS G12C inhibitor 47 shows p-ERK inhibition activities with IC50s of 0.046, 69.8 µM in MIA PaCA-2, A549 cells, respectively. KRAS G12C inhibitor 47 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS G12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRAS G12C inhibitor with an IC50 of 0.21 μM in KRAS G12C/SOS1 binding assay. KRAS G12C inhibitor 57 induces cancer cell apoptosis .
KRAS G12C inhibitor 39 is a potent inhibitor of KRAS G12C. KRas is a highly attractable target of the pharmaceutical industry for cancer research. KRAS G12C inhibitor 39 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2019099524A1, compound 494) .
KRAS G12C inhibitor 35 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 35 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent CN112920183A, compound 3) .
KRAS G12C inhibitor 41 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 41 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2021129824A1, compound 121) .
KRAS G12C inhibitor 40 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 40 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2021129824A1, compound 70) .
KRAS G12C inhibitor 37 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 37 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2018143315A1, compound 65) .
KRAS G12C inhibitor 38 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 38 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2021129820A1, compound 171) .
KRAS G12C inhibitor 42 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 42 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2020146613A1, compound 10) .
KRAS G12C inhibitor 61 (Example 3) inhibits phospho-ERK 1/2 in MIA PaCa-2 cells with an IC50 value of 9 nM. KRAS G12C inhibitor 61 can be used for research of pancreatic, colorectal, and lung cancers .
KRASG12C IN-12 (compound-1) is a KRAS G12C inhibitor. KRASG12C IN-12 (compound-1) can form a ternary complex with intracellular CYPA and the activated KRAS G12C mutant .
Glecirasib (Compound 1-2; JAB-21822) is an orally active and potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. Glecirasib has the potential for the research of KRAS G12C-mediated cancer .
KRASG12C IN-13 (LY3499446) is a potent KRAS G12C inhibitor. KRASG12C IN-13 is promising for research of advanced solid tumors including non-small cell lung cancer and colorectal cancer .
KRASG12C IN-14 (compound 15) is an inhibitor targeting the KRAS G12C mutation. KRASG12C IN-14 inhibits CYPA-dependent KRAS-BRAF with an IC50 of 0.002 μM. KRASG12C IN-14 inhibits ERK phosphorylation in NCI-H358 cells with an IC50 of 0.002 μM .
PROTAC KRAS G12C degrader-2 (compound 432) is a modulator of K-Ras protein hydrolysis. PROTAC KRAS G12C degrader-2 is a bifunctional compound, which contain on one end a cereblon inhibitor of apoptosis proteins (IAP) and on the other end a moiety which binds KRAS .
Sotorasib (AMG-510) is a first-in-class, orally bioavailable, and selective KRAS G12C covalent inhibitor. Sotorasib irreversibly inhibits KRAS G12C by locking it in an inactive GDP-bound state. Sotorasib is the first KRAS G12C inhibitor in clinical development and leads to the regression of KRAS G12C tumors .
TH-Z827 is a mutant selective KRAS(G12D) inhibitor with an IC50 of 2.4 μM. TH-Z827 does not bind KRAS(WT) or KRAS(G12C). TH-Z827 blocked the KRAS(G12D)-CRAF interaction with an IC50 value of 42 μM .
BBO-8520 is a direct small molecule covalent inhibitor targeting KRAS G12C with high oral availability. BBO-8520 has the characteristics of KRAS G12C (OFF) inhibitor and the function of blocking KRAS G12C (ON) signal. BBO-8520 inhibits cell proliferation by inhibiting KRAS G12C (ON) by binding GTP protein. BBO-8520 can block RAS-RAF1 interaction and return KRAS G12C to the inactive (OFF) state .
Pomalidomide-C12-NH2 hydrochloride is the E3 ligase ligand-linker conjugate of PROTAC KRAS G12C degrader-1 (HY-139186). PROTAC KRAS G12C degrader-1 is a Cereblon-based KRAS G12C degrader .
LC-2 is a potent and first-in-class von Hippel-Lindau-based PROTAC capable of degrading endogenous KRAS G12C, with DC50s between 0.25 and 0.76 μM . LC-2 covalently binds KRAS G12C with a MRTX849 warhead and recruits the E3 ligase VHL, inducing rapid and sustained KRAS G12C degradation leading to suppression of MAPK signaling in both homozygous and heterozygous KRAS G12C cell lines .
ASP2453 is a potent, selective and covalent KRAS G12C inhibitor. ASP2453 inhibits the Son of Sevenless (SOS)-mediated interaction between KRAS G12C and Raf with an IC50 value of 40 nM.
YF135 is an efficient and reversible-covalent KRAS G12C PROTAC. YF135 is designed and synthesized by tethering KRAS G12C inhibitor 48 (compound 6d) as the ligand, and basing on the scaffold of MRTX849 linkage VHL ligand. YF135 significantly induces the degradation of KRAS G12C in a reversible manner and decreases phospho-ERK level through the E3 ligase VHL mediated proteasome pathway .
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 .
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state.
Sotorasib-d7 (AMG-510-d7) is a deuterium-labeled Sotorasib (HY-114277). Sotorasib is an orally active covalent inhibitor of KRAS G12C. Sotorasib can lead to the regression of KRAS G12C tumors .
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 .
Divarasib (GDC-6036) adipate is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state .
Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction .
MRTX849 ethoxypropanoic acid incorporates a ligand for KRAS G12C, and a PROTAC linker. MRTX849 ethoxypropanoic acid 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 (IC50s between 0.25 and 0.76 μM) .
RM-018 is a potent, functionally distinct tricomplex KRAS G12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRAS G12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRAS G12C .
RMC-6291 is an orally active and covalent inhibitor of KRAS G12C(ON). RMC-6291 forms a tri-complex within tumor cells between KRAS G12C(ON) and cyclophilin A (CypA). Thus, RMC-6291 prevents KRAS G12C(ON) from signaling via steric blockade of RAS effector binding. RMC-6291 inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. RMC-6291 also inhibits the proliferation of KRAS G12C mutant cells with a median IC50 of 0.11 nM .
AZD4625 (Compound 21) is a highly potent, selective, covalent and allosteric inhibitor of the mutant GTPase KRAS G12C. AZD4625 has high oral bioavailability .
MRTX-1257 is a selective, irreversible, covalent and orally active KRAS G12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
ASP6918 is a potent and orally active KRAS G12C inhibitor with an IC50 value of 0.028 µM. ASP6918 inhibits cell growth. ASP6918 shows antitumor activity .
CFL-137 is a potent KRas G12C inhibitor. CFL-137 shows an antiproliferative effect. CFL-137 shows anticancer activity. CFL-137 has the potential for the research of lung cancer .
CFL-120 is a potent KRas G12C inhibitor. CFL-120 shows an antiproliferative effect. CFL-120 shows anticancer activity. CFL-120 has the potential for the research of lung cancer .
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 KRas G12V, respectively .
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 .
MK-1084 is a selective KRAS G12C inhibitor that is currently in Phase I clinical trial (NCT05067283). MK-1084 exhibits anticancer activity and can be used either alone or in combination with pembrolizumab (HY-P9902) for cancer research .
DCC-3116 is an orally active ULK1/2 inhibitor. DCC-3116 can promote autophagy in lung cancer cells by inhibiting KRAS G12C signaling, thereby inhibiting the proliferation of lung cancer cells and exerting anti-cancer effects .
(9R,12aR)-AZD4747 is a diastereomer of AZD4747 (HY-154959). AZD4747 is a selective mutant GTPase KRAS G12C inhibitor with blood-brain barrier permeability. AZD4747 has the potential to study cancer .
(S)-JDQ-443 is an isomer of JDQ-443 (HY-139612). JDQ-443 is an orally active, potent, selective, and covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1). JDQ-443 shows antitumor activity .
YN14 is a KRASG12C proteolysis targeting chimera (PROTAC). YN14 is highly potent and selective KRASG12C degrader and induces a stable KRASG12C: YN14: VHL ternary complex with low binding free energy (ΔG). YN14 has antiproliferative effects and significantly inhibits KRASG12C-mutant cancer cell growth. YN14 leads to tumor regression with tumor growth inhibition (TGI%) rates more than 100 % in the MIA PaCa-2 xenograft model.
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) .
MRTX-1257-d6 is the deuterium labeled MRTX-1257 (HY-114436). MRTX-1257 is a selective, irreversible, covalent and orally active KRAS G12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
ARS-1323-alkyne, a switch-II pocket (S-IIP) inhibitor, is a conformational specific chemical reporter of KRAS G12C nucleotide state in living cells . ARS-1323-alkyne is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
(3R,10R,14aS)-AZD4625 is the isomer of AZD4625 (HY-146223), and can be used as an experimental control. AZD4625 (Compound 21) is a highly potent, selective, covalent and allosteric inhibitor of the mutant GTPase KRAS G12C. AZD4625 has high oral bioavailability .
K20 is a potent and selective KRas G12C inhibitor with an IC50 of 1.16 µM. K20 shows anticancer activity in H358 cells (IC50= 0.78 µM). K20 decreases the levels of phosphorylated Erk and leads to cancer cell apoptosis. K20 suppresses NCI-H358 tumor growth with a TGI of 41% without causing obvious toxicity .
KRAS inhibitor-13 (compound 5-6) is a potent KRAS G12C inhibitor with an IC50 of 0.883 µM. KRAS inhibitor-13 shows p-ERK inhibition activities with IC50s of 5.9, >100 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-13 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-12 (compound 6-1) is a potent KRAS G12C inhibitor with an IC50 of 0.537 µM. KRAS inhibitor-12 shows p-ERK inhibition activities with IC50s of 1.3, 3.7 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-12 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-14 (compound 3-22) is a potent KRAS G12C inhibitor with an IC50 of 0.249 µM. KRAS inhibitor-14 shows p-ERK inhibition activities with IC50s of 1.12, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-14 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-15 (compound 3-19) is a potent KRAS G12C inhibitor with an IC50 of 0.954 µM. KRAS inhibitor-15 shows p-ERK inhibition activities with IC50s of 2.03, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-15 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-16 (compound 3-11) is a potent KRAS G12C inhibitor with an IC50 of 0.457 µM. KRAS inhibitor-16 shows p-ERK inhibition activities with IC50s of 3.06, 11.1 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-16 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-17 (compound 3-9) is a potent KRAS G12C inhibitor with an IC50 of 3.37 µM. KRAS inhibitor-17 shows p-ERK inhibition activities with IC50s of 9.25, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-17 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRAS inhibitor-18 (compound 3-10) is a potent KRAS G12C inhibitor with an IC50 of 4.74 µM. KRAS inhibitor-18 shows p-ERK inhibition activities with IC50s of 66.4, 11.1 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-18 has the potential for the research of pancreatic, colorectal, and lung cancers .
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 .
BI-0474 is a potent KRAS G12C inhibitor with an IC50 value of 7.0 nM for the GDP-KRAS::SOS1 protein-protein interaction. BI-0474 exhibits good anti-proliferative activity against NCI-H358 cells carrying the G12C mutation. BI-0474 also shows good anti-tumour activity in non-small cell lung cancer xenograft models .
KRAS G12D inhibitor 25 (Compound 148) is an inhibitor for KRAS G12C and HSP90α with IC50 of < 0.1 μM and 0.1-1 μM, respectively. KRAS G12D inhibitor 25 inhibits the proliferation of MIA PaCa-2 and NCI-H358 with EC50 of < 0.1 μM and 0.1-1 μM, respectively. KRAS G12D inhibitor 25 degrades ERBB2 with a DC50 of 0.1-1 μM .
KRAS inhibitor-9, a potent KRAS inhibitor (Kd=92 μM), blocks the formation of GTP-KRAS and downstream activation of KRAS. KRAS inhibitor-9 binds to KRAS G12D, KRAS G12C and KRAS Q61H protein with a moderate binding affinity. KRAS inhibitor-9 causes G2/M cell cycle arrest and induces apoptosis. KRAS inhibitor-9 selectively inhibits the proliferation of NSCLC cells with KRAS mutation but not normal lung cells .
D3S-001 is an orally active inhibitor for KRAS. D3S-001 inhibits the proliferation of KRAS G12C mutant H358 and MIA-PA-CA-2 with an IC50 of 0.6 and 0.44 nM. D3S-001 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 .
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 KRAS G12V 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 .
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 .
SIAIS562055 is a potent cereblon-based SOS1 PROTAC with a Kd of 95.9 nM. SIAIS562055 exhibits sustained degradation of SOS1 and inhibition of downstream ERK pathways. SIAIS562055 effectively blocked the binding of KRAS G12C or KRAS G12D to SOS1, with the IC50 values of 95.7 nM and 134.5 nM, respectively. SIAIS562055 exhibits potent anticancer activity. (Pink: SOS1 ligand (HY-168638); Black: linker (HY-W539874); Blue: E3 ligase ligand (HY-W076696)) .
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 .
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.
HRX-0233 is a small-molecule MAP2K4 inhibitor. HRX-0233 results in strong tumor shrinkage without any apparent toxicity in H358 KRASG12C-mutant non-small cell lung cancers (NSCLC) in vivo. HRX-0233 efficiently prevents feedback activation of receptor tyrosine kinases (RTKs) upon monotherapy KRAS inhibitor Sotorasib (HY-114277) and causes a more sustained and complete inhibition of MAPK signaling. HRX-0233 is promising for research of AR-negative prostate cancer, lung and colon cancers .
(R)-BI-2852 is the isomer of BI-2852 (HY-126247), and can be used as an experimental control. 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.
HLA-A*1101as, a pivotal MHCI molecule, presents viral and tumor-derived peptides, guiding T cell immune responses against infected or transformed cells. Collaborating with B2M, it displays a diverse peptide repertoire. Both the presented peptide and MHCI contribute to antigen recognition specificity. HLA-A*1101 typically presents 8 to 13 amino acid intracellular peptides, binding different peptides with allele-specific motifs. It plays a crucial role in controlling infections, presenting immunodominant epitopes from HIV-1, EBV, HBV, and contributing to the immune response against SARS-CoV-2. HLA-A*1101 KRAS G12C Complex Protein, Human (Biotinylated, VVVGACGVGK, 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 VVVGACGVGK peptide. HLA-A*1101 KRAS G12C Complex Protein, Human (Biotinylated, VVVGACGVGK, HEK293, His-Avi), has molecular weight of 53-63 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 G12C Complex Protein, Human (VVVGACGVGK, 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 VVVGACGVGK peptide. HLA-A*1101 KRAS G12C Complex Protein, Human (VVVGACGVGK, HEK293, His-Avi), has molecular weight of 53-63 kDa.
Sotorasib-d7 (AMG-510-d7) is a deuterium-labeled Sotorasib (HY-114277). Sotorasib is an orally active covalent inhibitor of KRAS G12C. Sotorasib can lead to the regression of KRAS G12C tumors .
MRTX-1257-d6 is the deuterium labeled MRTX-1257 (HY-114436). MRTX-1257 is a selective, irreversible, covalent and orally active KRAS G12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
ARS-1323-alkyne, a switch-II pocket (S-IIP) inhibitor, is a conformational specific chemical reporter of KRAS G12C nucleotide state in living cells . ARS-1323-alkyne is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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 KRas G12V, respectively .
Inquiry Online
Your information is safe with us. * Required Fields.
