ERK Inhibitor

VEGFR2-IN-84 is an orally active, multi-targeted tyrosine kinase inhibitor based on a naphthalene ring scaffold. VEGFR2-IN-84 inhibits VEGFR2 with sub-nanomolar affinity and broadly targets kinases including Kit, FGFR, PDGFR, and Ret. By competitively binding to the ATP-binding pocket, VEGFR2-IN-84 blocks the phosphorylation of VEGFR2 and its downstream AKT/ERK signaling pathway, thereby significantly inhibiting endothelial cell proliferation, migration, and tumor angiogenesis. VEGFR2-IN-84 exhibits broad-spectrum antiproliferative activity against various solid tumors such as liver cancer, lung cancer, and renal cancer, shows weak toxicity to normal cells, and has superior potency to Lenvatinib (HY-10981). VEGFR2-IN-84 possesses favorable pharmacokinetic properties and high safety (LD₅₀>2000 mg/kg), and can be used in related studies of various malignant tumors.

LC-MG-5 is a selective molecular glue degrader targeting FGFR2, with a DC₅₀ of 231.7 nM in KATO III cells. LC-MG-5 induces proteasomal degradation of FGFR2 in a DCAF16-dependent manner via a covalent molecular glue mechanism. LC-MG-5 inhibits cancer cell proliferation. LC-MG-5 suppresses PI3K/AKT and MAPK/ERK signaling pathways mediated by FGFR2. LC-MG-5 can be used in the research of gastric cancer.

KRAS G12D-IN-27 (H12a) is an inhibitor of KRAS G12D. KRAS G12D-IN-27 inhibits ERK phosphorylation, with an IC₅₀ of 112 nM. KRAS G12D-IN-27 can be used in cancer research.

ERK1/2 inhibitor 10 (Compound 36c) is a potent ERK1 and ERK2 inhibitor (IC₅₀: 0.11 and 0.08 nM respectively). ERK1/2 inhibitor 10 inhibits ERK1/2 and blocks the phosphorylation expression of their downstream substrates p90RSK and c-Myc. ERK1/2 inhibitor 10 induces cell apoptosis and incomplete autophagy-related cell death. ERK1/2 inhibitor 10 shows potent antitumor efficacy against triple-negative breast cancer and colorectal cancer models harboring BRAF and RAS mutations.

ERK1/2 inhibitor 12 (compound 76.3) is a ERK1/2 inhibitor which inhibits ERK-mediated phosphorylation of caspase-9 and the p90Rsk-1 kinase. ERK1/2 inhibitor 12 exhibits anti-cancer activity and can be utilized in cancer research.

Myristoyl-MEK1 Derived Peptide Inhibitor 1 is the myristoylated form of the MEK1 Derived Peptide Inhibitor 1 (HY-P4133). Myristoyl-MEK1 Derived Peptide Inhibitor 1 inhibits ERK activation with an IC₅₀ of 10 μM.

Dodoviscin I (Dodoviscin A) is an adipogenic agent that increases triglyceride content in 3T3L1 mouse fibroblasts. Dodoviscin I inhibits ERK2 with an IC₅₀ of 10.79 μM.

ERK1/2 inhibitor 11 (compound L6) is a dual inhibitor of ERK1/2, lending to DSB accumulation and ERK1/2 expression degradation. ERK1/2 inhibitor 11 lowers the levels of BCL-2, and induces DNA damage by inhibiting PARP and ERK1/2. ERK1/2 inhibitor 11 activates caspase 3 to inducing apoptosis..

PROTAC SOS1 degrader-3 is a PROTAC degrader targeting SOS1, which induces the targeted degradation of SOS1 via the ubiquitin-proteasome system, with DC₅₀ values ranging from 0.19 μM to 0.75 μM in multiple distinct colorectal cancer cell lines. PROTAC SOS1 degrader-3 inhibits the phosphorylation of AKT and ERK. PROTAC SOS1 degrader-3 induces apoptosis and morphological changes in KRAS-mutant colorectal cancer organoids. PROTAC SOS1 degrader-3 can be applied in studies related to kras-mutant colorectal cancer.

CXJ-2 is a cyclic peptide, and exhibits moderate affinity toward elastin derived peptides (EDPs). CXJ-2 exhibits potent activities to inhibit the PI3K/ERK pathway and decrease hepatic stellate cell proliferation and migration. CXJ-2 possesses potent antifibrotic efficacy.

WB-308 is a novel small molecule that was identified as an inhibitor of EGFR by an in vitro EGFR kinase activity system. WB-308 was able to reduce the proliferation and clonogenicity of NSCLC cells, causing G2/M phase arrest and apoptosis. In addition, WB-308 inhibited tumor growth in two in vivo animal models (lung orthotopic transplantation model and patient-derived clonal mouse model). WB-308 impaired the phosphorylation of EGFR, AKT, and ERK1/2 proteins. Compared with Gefitinib, WB-308 had lower cytotoxicity. This study showed that WB-308 is a new EGFR-TKI that may be considered as an alternative to Gefitinib in the clinical treatment of NSCLC.

KRASG12C IN-19 is a selective and orally active KRAS^G12C inhibitor. KRASG12C IN-19 exerts potent antiproliferative activity against the KRAS^G12C-mutant non small cell lung cancer (NSCLC) cell line H358 with an IC₅₀ of 7.6 nM, and effectively suppresses downstream ERK phosphorylation (IC₅₀ = 24.06 nM). KRASG12C IN 19 has no significant inhibitory activity against KRAS^G12V and KRAS^G12D-mutant cancer cells (PANC 1, Panc, AsPC 1, and GP2d cells) with IC₅₀ > 10,000 nM. KRASG12C IN-19 rapidly forms a covalent bond with KRAS^G12V-GDP, leading to dose-dependent inhibition of the downstream KRAS pathway. KRASG12C IN 19 can be employed for research in KRAS^G12C driven cancers, including non small cell lung cancer, pancreatic cancer, and colorectal cancer.

7α,15-Dihydroxydehydroabietic acid is a natural abietane-type diterpenoid with antiangiogenic effects.

PCC0105005 is a dual-target CGRP Receptor antagonist (IC₅₀ = 1.01 nM) and a partial agonist of 5-HT1F Receptor (EC₅₀ = 77.91 nM). PCC0105005 shows significant efficacy in the rat model of migraine. PCC0105005 significantly reduces the expression of CGRP and c-Fos proteins, and inhibits the phosphorylation levels of ERK and CREB. PCC0105005 can be used for research on migraine.

X-370 is a PI3Kδ inhibitor (IC₅₀ = 7 nM). X-370 inhibits the survival of leukemia cells, inducing G1 arrest and apoptosis. X-370 blocks PDK1 binding and phosphorylation of MEK1/2, eliminating Akt and Erk1/2 signaling. X-370 can be used in research on B-cell acute lymphoblastic leukemia (B-ALL).

OR-1855 (Standard) is an analytical standard of OR-1855 (HY-W050000). This product is intended for research and analytical applications. OR-1855, an active metabolite of Levosimendan (HY-14286), has effect on myometrial contractility. OR-1855 exerts anti-inflammatory effects by inhibiting IL-1β-induced ROS formation and NAD(P)H oxidase-dependent superoxide radical generation in HUVECs. OR-1855 inhibits IL-1β-induced phosphorylation p38 MAPK, ERK1/2, c-Jun and JNK in HUVECs. OR-1855 can be used for the study of inflammation.

ERK5-IN-7 is an orally active ERK5 inhibitor with an IC₅₀ of 403.4 nM. ERK5-IN-7 directly inhibits ERK5 kinase activity, and downregulates the phosphorylation level and total protein expression of ERK5. ERK5-IN-7 induces Apoptosis (upregulates Bax, downregulates Bcl-2, and induces Caspase-3 cleavage). ERK5-IN-7 induces ROS accumulation. ERK5-IN-7 exhibits anticancer effects against Lewis lung cancer.

SAIT-301 is a Met-targeting monoclonal antibody. SAIT-301 inhibits Met activation, induces downregulated expression of phosphorylated Met(p-Met) and phosphorylated ERK(p-ERK), and reduces EGR-1 expression. SAIT-301 inhibits the migration and invasion of nasopharyngeal carcinoma cells. SAIT-301 is applicable to relevant research on nasopharyngeal carcinoma. For the isotype control of SAIT-301, refer to Human IgG1 kappa, Isotype Control (HY-P99001).

ERK2-IN-6 (Compound 20) is a highly selective ERK1/2 inhibitor with an IC₅₀ value of 7.9 nM for ERK2. ERK2-IN-6 inhibits the proliferation of BRAF^V600E mutant cells (IC₅₀=250 nM in A375 cells). ERK2-IN-6 is promising for research of solid tumors, such as BRAF-mutated melanoma.

Mogrol (Standard) is the analytical standard of Mogrol. This product is intended for research and analytical applications. Mogrol is a biometabolite of mogrosides, and acts via inhibition of the ERK1/2 and STAT3 pathways, or reducing CREB activation and activating AMPK signaling.