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SOS1agonist-1 (compound 79) is an agonist for the Son of sevenless homologue SOS1. SOS1 is a guanine nucleotide exchange factor that catalyzes the exchange of GDP to GTP on RAS and regulates RAS activation. SOS1 agonists increase nucleotide exchange on RAS, enhance cellular RAS-GTP levels, and trigger biphasic signaling changes in ERK1/2 phosphorylation. Play an anti-cancer role [1] .
SOS1 Ligand intermediate-3 (Compound 5) is an SOS1 binder that can be used together with pomalidomide (HY-10984) for the synthesis of SOS1 PROTACs [1].
SOS1 Ligand intermediate-5 is the ligand for son of sevenless 1(SOS1).SOS1 Ligand intermediate-5 is utilized for synthesis of PROTAC SOS1 degrader-10 (HY-161654) [1].
SOS1 activator 1 (Compound 64) is a potent activator of SOS1-mediated nucleotide exchange with a Kd of 44 nM. SOS1 is a guanine nucleotide exchange factor that catalyzes the exchange of GDP for GTP on RAS [1].
SOS1 Human Pre-designed siRNA Set A contains three designed siRNAs for SOS1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
SOS1-IN-12 is a potent son of sevenless homolog 1(SOS1) inhibitor with a Ki of 0.11 nM for SOS1 and an IC50 of 47 nM for pERK. SOS1-IN-13 can be used for researching anticancer [1].
SOS1-IN-13 is a potent son of sevenless homolog 1(SOS1) inhibitor with IC50s of 6.5 nM and 327 nM for SOS1 and pERK, respectively. SOS1-IN-13 can be used for researching anticancer [1].
SOS1-IN-16 (Comp 54) is a selective inhibitor of SOS1 with an IC50 of 7.2 nM. SOS1-IN-16 has inhibitory activity of CYP3A4 when using testosterone as a substrate, with an IC50 of 8.9μM. SOS1-IN-16 can be used for cancer research [1].
SOS1-IN-5 is a potent inhibitor of SOS1. SOS1-IN-5 is a pyrimidobicyclic derivative. SOS1-IN-5 blocks the activation of KRAS by interfering with RAS-SOS1 interaction, and achieves the purpose of broad-spectrum inhibition of KRAS activity. SOS1-IN-5 has the potential for the research of cancer diseases (extracted from patent WO2021203768A1, compound 4) [1].
SOS1-IN-3 is a potent SOS1 (son of sevenless homolog 1) inhibitor with an IC50 of 5 nM. SOS1-IN-3 has anticancer effects (WO2019122129A1; compound I-1) [1].
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) [1].
SOS1-IN-15 (Compound 37) is an orally active SOS1 inhibitor with an IC50 of 5 nM. SOS1-IN-15 is a promising agent candidate for the research of KRAS-driven cancer [1].
SOS1/EGFR-IN-1 (compound SE-9) is a dual-target inhibitor for the prostate cancer. SOS1/EGFR-IN-1 inhibits effectively SOS1(IC50=42.13±1.55 nM) and EGFR(IC50=1.01±0.04 nM) by inhibiting their downstream effector molecules. SOS1/EGFR-IN-1 induces apoptosis and G1 phase cell cycle arrest, reducing angiogenesis and migration. SOS1/EGFR-IN-1 shows significant antitumor effects in prostate cancer cells PC-3 (IC50=0.45±0.03 μM) [1].
VHL Ligand intermediate-2 (compound 18c) is an intermediate for the synthesis of VHL E3 ubiquitin ligase ligand and can be used to synthesize PROTACs [1].
VHL Ligand intermediate-1 (intermediate 18a) is an intermediate in the synthesis of VHL E3 ubiquitin ligase ligand and can be used to synthesize PROTACs [1].
PROTAC SOS1 degrader-3 is a potent PROTAC SOS1 degrader. PROTAC SOS1 degrader-3 effectively targeted SOS1 for degradation through the ubiquitin-proteasome system [1].
PROTAC SOS1 degrader-5 (compound 4) is a potent PROTAC SOS1 degrader, with the DC50 of 13 nM. PROTAC SOS1 degrader-5 strongly inhibits NCI-H358 cells proliferation with an IC50 of 5 nM [1].
PROTAC SOS1degrader-1 is a potent PROTAC SOS1 degrader with an DC50 of 98.4 nM. PROTAC SOS1degrader-1 shows antiproliferation activity in cancer cells with various KRAS mutations. PROTAC SOS1degrader-1 shows antitumor effect with low toxicity [1].
PROTAC SOS1degrader-1 (TFA) is a potent PROTAC SOS1 degrader with an DC50 of 98.4 nM. PROTAC SOS1degrader-1 shows antiproliferation activity in cancer cells with various KRAS mutations. PROTAC SOS1degrader-1 shows antitumor effect with low toxicity [1].
PROTAC SOS1 degrader-10 (Compound 11o) is a degrader for son of sevenless 1(SOS1) in a CRBN and proteasome dependent manner. PROTAC SOS1 degrader-10 degrades SOS1 in KRAS mutant cancer cells SW620, A549 and DLD-1, with DC50s of 2.23, 1.85 and 7.53 nM, respectively. PROTAC SOS1 degrader-10 inhibits the proliferations of cells SW620, A549 and DLD-1, with IC50s of 36.7, 52.2 and 107 nM, respectively. PROTAC SOS1 degrader-10 inhibits phosphorylation of ERK. (Pink: SOS1 ligand (HY-161655); Black: linker (HY-161656); Blue: E3 ligase ligand (HY-W249500)) [1]
(4S)-PROTAC SOS1degrader-1 is a potent PROTAC SOS1 degrader. (4S)-PROTAC SOS1degrader-1 decreases the expression of pERK and RAS-GTP level in a dose-dependent manner. (4S)-PROTAC SOS1degrader-1 significantly inhibits the tumor growth in vivo [1].
(4S)-PROTAC SOS1degrader-1 (diTFA) is a potent PROTAC SOS1 degrader. (4S)-PROTAC SOS1degrader-1 (diTFA) decreases the expression of pERK and RAS-GTP level in a dose-dependent manner. (4S)-PROTAC SOS1degrader-1 (diTFA) significantly inhibits the tumor growth in vivo [1].
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 [1].
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 [1].
BAY-293, a valuable chemical probe, blocks RAS activation via disruption of the KRAS-SOS1 interaction with an IC50 of 21 nM. BAY-293 is a potent inhibitor of Son of Sevenless 1(SOS1).SOS1 is the guanine nucleotide exchange factor (GEF) and activator of RAS [1].
KRAS ligand 4 (Compound 2) is a bifunctional depressant based on SOS1. KRAS ligand 4 reduces the downstream signaling markers pERK and pS6 and shows anti-proliferative activity in multiple KRAS mutated cells [1].
BTX-6654 is a target-dependent and -specific cereblon-based bifunctional SOS1PROTAC degrader. BTX-6654 reduces downstream signaling markers pERK and pS6, and displays antiproliferative activity in cells harboring various KRAS mutations [1].
RMC-0331 (RM-023) is a potent, selective and orally bioavailable SOS1 inhibitor. RMC-0331 is an in vivo tool compound that blocks RAS activation via disruption of the RAS-SOS1 interaction [1].
LHF418 is an effective SOS1 PROTAC degrader with a DC50 value of 209.4 nM in A549 cells. LHF418 can effectively inhibit RAS signaling and colony formation in KRAS-driven cancer cells. (Structural note: (Blue: Cereblon ligand (HY-A0003), Black: linker; Pink: SOS1 binder SOS1 Ligand intermediate-3 (HY-161452)) [1].
BI-3406 (compound I-6) is an orally active, highly potent and selective inhibitor of the interaction between KRAS and Son of Sevenless 1(SOS1) with an IC50 of 6 nM. BI-3406 potently reduces the formation of GTP-loaded KRAS, and inhibits MAPK pathway signaling. BI-3406 has anticancer activity [1] .
UC-857993 is a selective SOS1-Ras inhibitor (Kd=14.7 μM, His6-SOS1cat), suppressing catalytic activity. UC-857993 also inhibits ERK and Ras activation, suppresses the growth of mouse embryonic fibroblasts (MEFs) [1].
NSC-70220 is a selective and allosteric SOS1 inhibitor. NSC-70220 inhibits allosteric site activation, and partially inhibited catalytic site activation. NSC-70220 has an anticancer effect [1].
BTX-7312 is a SOS1 cereblon-based bifunctional degrader. BTX-7312 reduces downstream signaling markers, pERK and pS6, and displays antiproliferative activity in cells harboring various KRAS mutations [1].
2-Methoxyphenyl dihydrouracil-azaspiro[5.5]undecane-C-PIP is an E3 Ligase ligand-linker conjugate, and can be used for synthesis of PROTAC SOS1 degrader-10 (HY-161654) [1].
PIP-C-3-Azaspiro[5.5]undecane-boc is the linker for PROTAC. PIP-C-3-Azaspiro[5.5]undecane-boc is utilized for synthesis of PROTAC SOS1 degrader-10 (HY-161654) [1].
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[1].
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 [1].
MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated KD against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations [1] .
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 [1].
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 [1].
SOS1 Antibody (YA3313) is a rabbit-derived non-conjugated IgG antibody (Clone NO.: YA3313), targeting SOS1, with a predicted molecular weight of 152 kDa (observed band size: 152 kDa). SOS1 Antibody (YA3313) can be used for WB, IHC-P, ICC/IF experiment in human, mouse, rat background.
MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated KD against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations [1] .
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