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KRASG12C inhibitor 39 is a potent inhibitor of KRASG12C. KRas is a highly attractable target of the pharmaceutical industry for cancer research. KRASG12C inhibitor 39 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2019099524A1, compound 494) .
KRASG12C inhibitor 35 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 35 has the potential for the research of KRASG12C-mediated cancer (extracted from patent CN112920183A, compound 3) .
KRASG12C inhibitor 41 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 41 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2021129824A1, compound 121) .
KRASG12C inhibitor 40 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 40 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2021129824A1, compound 70) .
KRASG12C inhibitor 37 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 37 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2018143315A1, compound 65) .
KRASG12C inhibitor 38 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 38 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2021129820A1, compound 171) .
KRASG12C inhibitor 42 is a potent inhibitor of KRASG12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRASG12C inhibitor 42 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2020146613A1, compound 10) .
KRASG12C inhibitor 61 (Example 3) inhibits phospho-ERK 1/2 in MIA PaCa-2 cells with an IC50 value of 9 nM. KRASG12C inhibitor 61 can be used for research of pancreatic, colorectal, and lung cancers .
Glecirasib (Compound 1-2; JAB-21822) is an orally active and potent inhibitor of KRASG12C. 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 KRASG12C-mediated cancer .
KRASG12C inhibitor 62 is a KRASG12C inhibitor. KRASG12C inhibitor 62 has the potential for the research of KRASG12C-mediated cancer (extracted from patent WO2021121367A1) .
KRASG12C inhibitor 57 (Compound 50) is a potent, selective, covalent and orally active KRASG12C inhibitor with an IC50 of 0.21 μM in KRASG12C/SOS1 binding assay. KRASG12C inhibitor 57 induces cancer cell apoptosis .
KRASG12C inhibitor 29 is a KRASG12C inhibitor extracted from patent WO2021252339A1, compound 3. KRASG12C inhibitor 29 can be used for the research of cancer .
KRASG12C inhibitor 30 is a KRASG12C inhibitor extracted from patent WO2021252339A1, compound 2. KRASG12C inhibitor 30 can be used for the research of cancer .
KRASG12C inhibitor 31 is a KRASG12C inhibitor extracted from patent WO2021252339A1, compound 1. KRASG12C inhibitor 31 can be used for the research of cancer .
KRASG12C inhibitor 33 is a KRASG12C inhibitor extracted from patent WO2021244603A1, compound 1. KRASG12C inhibitor 33 can be used for the research of cancer .
KRASG12C inhibitor 34 is a KRASG12C inhibitor extracted from patent WO2021239058A1, compound Z1. KRASG12C inhibitor 34 can be used for the research of cancer .
KRASG12C inhibitor 60 (compound 23) is a Kras-G12C inhibitor. KRASG12C inhibitor 60 can be used for the research of lung cancer, colorectal cancer, pancreatic cancer .
KRASG12C inhibitor 44 (compound 54) is a potent and orally active KRASG12C inhibitor. KRASG12C inhibitor 44 shows anti-proliferation activities with IC50s of 0.016, 0.028 µM in MIA PaCA-2, H358 cells, respectively. KRASG12C inhibitor 44 shows antitumor effects in vivo .
KRASG12C inhibitor 65 is a potent and covalent KRASG12C inhibitor that traps KRASG12C in the GDP-bound state. KRASG12C IN-1 exhibits potent antitumor activity against KRAS-mutant non-small cell lung cancer .
KRASG12C inhibitor 47 (compound 8-1-1) is a potent KRASG12C inhibitor with an IC50 of 0.172 µM. KRASG12C inhibitor 47 shows p-ERK inhibition activities with IC50s of 0.046, 69.8 µM in MIA PaCA-2, A549 cells, respectively. KRASG12C inhibitor 47 has the potential for the research of pancreatic, colorectal, and lung cancers .
KRASG12C inhibitor 48 (compound 6e) is a potent KRASG12C inhibitor with an IC50 of 639.91 nM. KRASG12C inhibitor 48 (0-50 µM) shows anti-proliferative activity with IC50s of 0.796, 6.33, 16.14 µM for H358, H23, A549 cells, respectively .
KRASG12C IN-14 (compound 15) is an inhibitor targeting the KRASG12C 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 .
KRASG12C IN-13 (LY3499446) is a potent KRASG12C inhibitor. KRASG12C IN-13 is promising for research of advanced solid tumors including non-small cell lung cancer and colorectal cancer .
KRASG12C IN-12 (compound-1) is a KRASG12C inhibitor. KRASG12C IN-12 (compound-1) can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant .
PROTAC KRASG12C degrader-2 (compound 432) is a modulator of K-Ras protein hydrolysis. PROTAC KRASG12C 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 .
Pomalidomide-C12-NH2 hydrochloride is the E3 ligase ligand-linker conjugate of PROTAC KRASG12C degrader-1 (HY-139186). PROTAC KRASG12C degrader-1 is a Cereblon-based KRASG12C degrader .
Sotorasib (AMG-510) is a first-in-class, orally bioavailable, and selective KRASG12C covalent inhibitor. Sotorasib irreversibly inhibits KRASG12C by locking it in an inactive GDP-bound state. Sotorasib is the first KRASG12C inhibitor in clinical development and leads to the regression of KRASG12C tumors .
RM-018 is a potent, functionally distinct tricomplex KRASG12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRASG12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRASG12C .
Sotorasib racemate (Compound A) is an orally active racemate of Sotorasib (HY-114277), a covalent inhibitor of KRASG12C mutant which induces adaptive feedback activation of MAPK pathway. Sotorasib racemate also exerts inhibitor activity against KRASG12C induced cancer and can be applied to 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, KRasG12C and KRas G12V, respectively .
MRTX849 ethoxypropanoic acid incorporates a ligand for KRASG12C, 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 KRASG12C (IC50s between 0.25 and 0.76 μM) .
Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRASG12C with potential antineoplastic activity. Adagrasib covalently binds to KRASG12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction .
MRTX-1257 is a selective, irreversible, covalent and orally active KRASG12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
BBO-8520 is a direct small molecule covalent inhibitor targeting KRASG12C with high oral availability. BBO-8520 has the characteristics of KRASG12C (OFF) inhibitor and the function of blocking KRASG12C (ON) signal. BBO-8520 inhibits cell proliferation by inhibiting KRASG12C (ON) by binding GTP protein. BBO-8520 can block RAS-RAF1 interaction and return KRASG12C to the inactive (OFF) state .
ARS-853 is a cell-active, selective, covalent KRASG12C 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 .
LC-2 is a potent and first-in-class von Hippel-Lindau-based PROTAC capable of degrading endogenous KRASG12C, with DC50s between 0.25 and 0.76 μM . LC-2 covalently binds KRASG12C with a MRTX849 warhead and recruits the E3 ligase VHL, inducing rapid and sustained KRASG12C degradation leading to suppression of MAPK signaling in both homozygous and heterozygous KRASG12C cell lines .
ASP2453 is a potent, selective and covalent KRASG12C inhibitor. ASP2453 inhibits the Son of Sevenless (SOS)-mediated interaction between KRASG12C and Raf with an IC50 value of 40 nM.
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 KRASG12C (DC50s between 0.25 and 0.76 μM) .
YF135 is an efficient and reversible-covalent KRASG12C PROTAC. YF135 is designed and synthesized by tethering KRASG12C inhibitor 48 (compound 6d) as the ligand, and basing on the scaffold of MRTX849 linkage VHL ligand. YF135 significantly induces the degradation of KRASG12C 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 KRASG12C mutant. RMC-4998 can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant, with an IC50 value of 28 nM. RMC-4998 can inhibit ERK signaling in KRASG12C mutant cancer cells and induce apoptosis. RMC-4998 can be used for tumor research .
MRTX-1257-d6 is the deuterium labeled MRTX-1257 (HY-114436). MRTX-1257 is a selective, irreversible, covalent and orally active KRASG12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
RMC-6291 is an orally active and covalent inhibitor of KRASG12C(ON). RMC-6291 forms a tri-complex within tumor cells between KRASG12C(ON) and cyclophilin A (CypA). Thus, RMC-6291 prevents KRASG12C(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 KRASG12C mutant cells with a median IC50 of 0.11 nM .
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRASG12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRASG12C 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 KRASG12C. Sotorasib can lead to the regression of KRASG12C tumors .
Divarasib (GDC-6036) adipate is an orally bioavailable, highly potent, and selective KRASG12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRASG12C and irreversibly locks it in the inactive GDP-bound state .
BI-0474 is a potent KRASG12C 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 .
AZD4625 (Compound 21) is a highly potent, selective, covalent and allosteric inhibitor of the mutant GTPase KRASG12C. AZD4625 has high oral bioavailability .
ASP6918 is a potent and orally active KRASG12C inhibitor with an IC50 value of 0.028 µM. ASP6918 inhibits cell growth. ASP6918 shows antitumor activity .
KRAS inhibitor-22 (compound FB9/6B9) is a potent inhibitor of K-Ras. KRAS inhibitor-22 targets to Kras 4B(G12D) and (G12C), which can be used for cancer research .
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 .
CFL-137 is a potent KRasG12C 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 KRasG12C 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-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 KRASG12C, 0.37 μM for KRAS G12D, 0.74 μM for KRAS Q61H). KRAS inhibitor-3 also disrupts interaction of KRAS with Raf .
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 .
MK-1084 is a selective KRASG12C 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 KRASG12C signaling, thereby inhibiting the proliferation of lung cancer cells and exerting anti-cancer effects .
KRAS inhibitor-13 (compound 5-6) is a potent KRASG12C 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 .
(9R,12aR)-AZD4747 is a diastereomer of AZD4747 (HY-154959). AZD4747 is a selective mutant GTPase KRASG12C inhibitor with blood-brain barrier permeability. AZD4747 has the potential to study cancer .
KRAS inhibitor-12 (compound 6-1) is a potent KRASG12C 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 KRASG12C 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 KRASG12C 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 KRASG12C 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 KRASG12C 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 KRASG12C 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 .
(S)-JDQ-443 is an isomer of JDQ-443 (HY-139612). JDQ-443 is an orally active, potent, selective, and covalent KRASG12C inhibitor (extracted from patent WO2021120890A1). JDQ-443 shows antitumor activity .
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, KRASG12C 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 .
SML-10-70-1 is a ligand for RAS, which covalently modifies the K-RasG12C 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 .
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 .
ARS-1323-alkyne, a switch-II pocket (S-IIP) inhibitor, is a conformational specific chemical reporter of KRASG12C 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 KRASG12C. AZD4625 has high oral bioavailability .
K20 is a potent and selective KRasG12C 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 .
MEK/RAF-IN-1 (Compound 16b) is an inhibitor of both MEK and RAF. It shows potent inhibition with IC50 values of 28 nM for MEK1, and 3 nM each for BRAF and BRAFV600E. MEK/RAF-IN-1 demonstrates significant antitumor activity, effectively inhibiting cell proliferation in vitro against MIA PaCa-2 (G12CKRAS), HCT116 (G13D KRAS), and C26 (G12D KRAS) cells. Additionally, it inhibits tumor growth in xenograft mouse models of colorectal cancer .
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 .
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 .
D3S-001 is an orally active inhibitor for KRAS. D3S-001 inhibits the proliferation of KRASG12C 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 .
GNE-7883 is a pan-TEAD inhibitor that blocks the association of YAP/TAZ with TEAD. GNE-7883 effectively reduces chromatin accessibility at TEAD motifs, inhibits cell proliferation in multiple cell line models, and achieves strong anti-tumor efficacy in vivo. In addition, GNE-7883 effectively overcomes intrinsic and acquired resistance to KRAS (Kirsten rat sarcoma viral oncogene homolog) G12C inhibitors in multiple preclinical models by inhibiting YAP/TAZ activation .
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 KRASG12C, G12D, and G12V are 1.3 nM, 4.7 nM, and 0.3 nM, respectively .
KRAS G12D inhibitor 11 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 11 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 52) .
KRAS G12D inhibitor 12 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 12 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 134) .
KRAS G12D inhibitor 9 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 9 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 20) .
KRAS G12D inhibitor 10 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 10 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 34) .
KRAS G12D inhibitor 13 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 13 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 142) .
KRAS G12D inhibitor 8 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 8 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021107160A1, compound 2) .
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 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 .
SOS1-IN-14 is a potent, selective and orally active SOS1 inhibitor with an IC50 value of 3.9 nM. SOS1-IN-14 can be absorbed in the intestine via a P-glycoprotein-mediated efflux mechanism. SOS1-IN-14 can be used to research KRAS-mutated cancers. SOS1-IN-14 has better potent tumor suppression than BI-3406 (HY-125817) .
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 .
KRAS Protein, Human (G12C, His) expresses in E. coli with a His tag at the N-terminus. KRAS G12C is an oncogenic driver mutation in multiple cancer types.
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 (G12C, His) is the recombinant human-derived Kras4B protein, expressed by E. coli , with N-6*His labeled tag and G12C, , , , mutation. The total length of Kras4B Protein, Human (G12C, His) is 169 a.a., with molecular weight of ~23.0 kDa.
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.
MRTX-1257-d6 is the deuterium labeled MRTX-1257 (HY-114436). MRTX-1257 is a selective, irreversible, covalent and orally active KRASG12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells .
Sotorasib-d7 (AMG-510-d7) is a deuterium-labeled Sotorasib (HY-114277). Sotorasib is an orally active covalent inhibitor of KRASG12C. Sotorasib can lead to the regression of KRASG12C tumors .
ARS-1323-alkyne, a switch-II pocket (S-IIP) inhibitor, is a conformational specific chemical reporter of KRASG12C 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, KRasG12C and KRas G12V, respectively .
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