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[1].

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[1].

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)[1].

KRAS G12D inhibitor 18 is a potent KRAS G12D inhibitor[1].

KRAS G12D inhibitor 18 is a potent KRAS G12D inhibitor[1].

KRAS G12D inhibitor 18 is a potent KRAS G12D inhibitor[1].

KRAS G12D inhibitor 19 (Compound 7) is a KRAS G12D inhibitor. KRAS G12D inhibitor 19 can be used for the research of cancer[1].

KRAS G12D modulator-1 (compound 6) is a potent KRAS G12D modulator with IC50 values of 1-10 μM for NEA-G12D, PPI-G12D, and p ERK-AGS, respectively. KRAS G12D modulator-1 can be used in research of cancer[1].

KRAS G12D 8-16 is a mutant KRAS G12D 8-16 peptide[1].

KRAS G13D-IN-1 (compound 41) is a selective and covalently reversible inhibitor of KRASG13D (IC50: 0.41 nM). The selectivity for KRASG13D is 29-fold against KRAS wild type. KRAS G13D-IN-1 is an inhibitor of the GDP state and targets the SWII binding pocket of KRASG13D. KRAS G13D-IN-1 inhibits KRAS binding to GDP and turns on/off downstream signaling […]

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[1].

KRAS inhibitor-23 (Isomer 2 of compound i) is a potent inhibitor of KRAS that plays an important role in cancer research[1].

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[1].

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[1].

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[1].

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[1].

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[1].

KRAS ligand 3 (compound 1) is BTX-6654 target-binding ligand that can bind KRAS inhibitor and diaplay synergistic tumor growth inhibiton[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].

KRASG12C IN-2 (compound 17) is an orally active KRASG12C inhibitor. KRASG12C IN-2 inhibits tumor growth in mice[1].

KRASG12D-IN-1 (compound 22) is a KRASG12D Inhibitor. KRASG12D-IN-1 has dose-dependent anti-tumor efficacy in the AsPC-1 xenograft mouse models with a tumor growth inhibition[1].

KRASG12D-IN-1 (compound 22) is a KRASG12D Inhibitor. KRASG12D-IN-1 has dose-dependent anti-tumor efficacy in the AsPC-1 xenograft mouse models with a tumor growth inhibition[1].

KRASG12D-IN-2 (compound 28) is a KRASG12D Inhibitor. KRASG12D-IN-1 has dose-dependent anti-tumor efficacy in the AsPC-1 xenograft mouse models with a tumor growth inhibition[1].

KRASG12D-IN-2 (compound 28) is a KRASG12D Inhibitor. KRASG12D-IN-1 has dose-dependent anti-tumor efficacy in the AsPC-1 xenograft mouse models with a tumor growth inhibition[1].

KRASG12D-IN-2 (compound 28) is a KRASG12D Inhibitor. KRASG12D-IN-1 has dose-dependent anti-tumor efficacy in the AsPC-1 xenograft mouse models with a tumor growth inhibition[1].

KRB-456 is a small molecule that binds a dynamic allosteric binding pocket within the switch-I/II region of KRAS G12D. KRB-456 inhibits P-MEK, P-AKT, and P-S6 levels in vivo and inhibits the growth of cancer. KRB-456 can be used for the research of pancreatic cancer[1].

KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach[1].

KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach[1].

KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach[1].

KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach[1].

KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach[1].

KRN5500 (NSC 650426), a Spicamycin (HY-127130) derivative and a nucleoside-like antibiotic with anti-tumor activity. KRN5500 also induces apoptosis via the down-regulation of Bcl-2 expression. KRN5500 shows a significant efficacy in the human tumor xenograft model in mice[1][2].

KRPpSQRHGSKY-NH2 is a biological active peptide. (This is a phosphorylated PKC substrate peptide)

KRpTIRR is a biological active peptide. (Phosphatase substrate.)

KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy[1][2].

KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy[1][2].

KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy[1][2].

KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy[1][2].

KSCM-11 is a ligand of thesigma receptor[1].

KSDSC is a penta-peptide, correlated positively with hairpin DNA with tetramer loops. Therefore, KSDSC joins hands with hairpin DNA (hpDNA) with improved selectivity as sensing materials in the detection system, used for surface plasmon resonance imaging (SPRi)[1].

KSDSC TFA is a penta-peptide, correlated positively with hairpin DNA with tetramer loops. Therefore, KSDSC TFA joins hands with hairpin DNA (hpDNA) with improved selectivity as sensing materials in the detection system, used for surface plasmon resonance imaging (SPRi)[1].

KSDSC TFA is a penta-peptide, correlated positively with hairpin DNA with tetramer loops. Therefore, KSDSC TFA joins hands with hairpin DNA (hpDNA) with improved selectivity as sensing materials in the detection system, used for surface plasmon resonance imaging (SPRi)[1].

KSI-3716-d4 is the deuterium labeled KSI-3716 (HY-12703)[1][2].

KSK67 is a high-affinity dual sigma-2 and histamine H3 receptor antagonist, with Kis of 3.2, 1531, 101 nM for H3 receptor, sigma-1, sigma-2 receptor respectively. KSK67 can be used for research of nociceptive and neuropathic pain[1].

KSK68 is a high-affinity dual sigma-1 and histamine H3 receptor antagonist, with Kis of 7.7, 3.6, 22.4 nM for H3 receptor, sigma-1, sigma-2 receptor respectively. KSK68 has negligible affinity at the other histamine receptor subtypes. KSK68 can be used for research of nociceptive and neuropathic pain[1].