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VUBI1 (SOS1 activator 1) is a benzimidazole derivative and SOS1 activator with a Kd of 44 nM. VUBI1 can significantly activate RAS-GTP and regulate the phosphorylation of ERK. VUBI1 also can serve as a target ligand for synthesizing PROTACs, such as PROTAC SOS1degrader-1 (HY-145737), to induceSOS1 degradation. VUBI1 can be used in the study of cancer [1] .
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 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 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 Ligand intermediate-7 (65) is an intermediate for the synthesis of SOS1 ligand (HY-111671). SOS1 activator 1 (HY-111671) can be used for the synthesis of PROTAC SOS1degrader-1 (HY-145737) [1].
SOS1 activator 2 (Compound 65) is a benzimidazole derivative and a SOS1 activator. SOS1 activator 2 has a high binding affinity for SOS1 with a Kd of 9 nM. SOS1 activator 2 can regulate the Ras-ERK signaling pathway, which can be used in the study of cancer [1].
Sos1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sos1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
Sos1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Sos1 gene (Mouse), 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-19 (Compound 10i) is a potent inhibitor of SOS1 (Son of Sevenless 1) with an IC50 value of 165.2 nM. SOS1-IN-19 blocks KRAS activation by preventing GDP/GTP exchange in KRAS signaling pathway. SOS1-IN-19 is promising for research of KRAS-driven cancers (e.g., NSCLC and colorectal cancer) [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-22 is a son of sevenless homolog 1(SOS1) inhibitor. SOS1-IN-22 can inhibit KRAS-G12C/SOS1 complex formation with an IC50 value of 40.28 nM. SOS1-IN-22 can reduce phosphorylation ERK levels. SOS1-IN-22 can be used for the research of cancer, such as pancreatic carcinoma and appendiceal carcinoma [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-20 (Compound 12f) is an orally active SOS1 inhibitor with an IC50 of 5.11 nM against KRAS G12C::SOS1. By disrupting the interaction between KRAS and SOS1, SOS1-IN-20 inhibits KRAS activation and downstream signal transduction. SOS1-IN-20 has an IC50 of 253 nM for p-ERK in PC-9 cells and 16.71 μM for hERG channel . SOS1-IN-20 can inhibit the proliferation of tumor cells and has antitumor activity [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-IN-18 (Compound 8) is the inhibitor for Son of Sevenless 1 protein(SOS1) with a KD of 2.6 nM, and inhibits SOS1-KRAS G12C interaction with an IC50 of 3.4 nM. SOS1-IN-18 inhibits the phosphorylation of ERK in H358 with an IC50 of 31 nM, inhibits the proliferation of H358 with an IC50 of 5 nM [1].
SOS1-IN-21 is an orally active inhibitor of son of Sevenless 1(SOS1) with an IC50 of 15 nM. SOS1 is a guanine nucleotide exchange factor (GEF) that activates KRAS by facilitating the exchange of GDP for GTP. SOS1-IN-21 exhibits potent antiproliferative activity, with IC50 values of 16 nM in NCI-H358 and 17 nM in Mia Paca-2 cell proliferation assays. SOS1-IN-21 exhibits significant antitumor activity in the Mia Paca-2 xenograft model. SOS1-IN-21 can be used for the study of KRAS mutant tumors, such as pancreatic cancer [1].
SOS1-IN-17 (Compound 8d) is an orally active inhibitor for SOS1-KRASG12C interaction with an IC50 of 5.1 nM. SOS1-IN-17 inhibits ERK phosphorylation in DLD-1 cell with an IC50 of 18 nM. SOS1-IN-17 exhibits anti-proliferative activity in KRASG12C mutated Mia-Paca-2 cell with an IC50 of 0.11 μM. SOS1-IN-17 exhibits antitumor efficacy against pancreatic cancer in mouse model [1].
SOS1/EGFR-IN-2 (Compound 4) is a SOS1 and EGFR dual inhibitor with IC50s of 8.3 and 14.6 nM, respectively. SOS1/EGFR-IN-2 exhibits significant antiproliferative effect on the cancer cells haboring various KRAS mutants [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-1 (intermediate 18a) is an intermediate in the synthesis of VHL E3 ubiquitin ligase ligand and can be used to synthesize PROTACs [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].
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].
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)) [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].
RGT-018 is a potent and orally active SOS1 inhibitor with anti-tumor effects. RGT-018 exerts anti-cancer cell proliferation activity by inhibiting KRAS activation [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].
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].
KRAS ligand 4 (compound 2) is a bifunctional molecular glue degrader based on SOS1. KRAS ligand 4 reduces downstream signaling markers pERK and pS6 and displays anti-additional activity in cells with multiple 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] .
SOF-436 is a KRAS inhibitor that inhibits SOS1-mediated KRAS nucleotide exchange (IC50 = 60 μM) and the binding of KRAS to the effector protein RAF. SOF-436 can be used in cancer research [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 cereblon-based SOS1 bifunctional degrader and a molecular glue. BTX-7312 reduces downstream signaling markers pERK and pS6 and shows antiproliferative activity in various KRAS-mutated cells [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].
KRASG12C IN-15 (Compound 21) is the orally active inhibitor for KRAS G12C, and inhibits SOS1-mediated GDP/GTP exchange with an IC50 of 19 nM. KRASG12C IN-15 inhibits the phosphorylation of ERK with IC50 of 0.051 μM. KRASG12C IN-15 inhibits the cell viability of KRAS G12C mutated MIA PaCa-2 with IC50 of 0.023 μM. KRASG12C IN-15 exhibits antitumor effect in MIA PaCa-2 xenograft mouse models [1].
MRTX1133 formic is a noncovalent, potent, and selective KRAS G12D inhibitor. MRTX1133 formic 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 formic prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRASG12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 formic shows efficacy in tumor models harboring KRAS G12D mutations [1] .
MRTX1133 is a noncovalent, potent, and selective alkyne-based 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] .
Sos2 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sos2 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
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].
MRTX1133 is a noncovalent, potent, and selective alkyne-based 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] .
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 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sos1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
Sos1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Sos1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
Sos2 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sos2 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
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