Search Result

Results for "

MEK-IN-1

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (4) Apoptosis (12) Autophagy (6) c-Met/HGFR (1) Calcium Channel (1) Caspase (1) CDK (1) Drug Derivative (1) E3 Ligase Ligand-Linker Conjugates (1) EGFR (1) ERK (8) FLT3 (2) Glutathione S-transferase (1) Isotope-Labeled Compounds (2) JNK (1) Keap1-Nrf2 (1) Ligands for Target Protein for PROTAC (1) MEK (36) NO Synthase (1) p38 MAPK (2) PARP (2) PDGFR (2) PDK-1 (1) PERK (1) PI3K (1) Pim (1) PKC (1) PROTACs (1) Raf (1) Reference Standards (6) SOD (1) Topoisomerase (1) VEGFR (3)
By Research Areas:	Cancer (43) Cardiovascular Disease (2) Inflammation/Immunology (8) Metabolic Disease (3) Neurological Disease (5)

By Targets:

Akt (4)

Apoptosis (12)

Autophagy (6)

c-Met/HGFR (1)

Calcium Channel (1)

Caspase (1)

CDK (1)

Drug Derivative (1)

E3 Ligase Ligand-Linker Conjugates (1)

EGFR (1)

ERK (8)

FLT3 (2)

Glutathione S-transferase (1)

Isotope-Labeled Compounds (2)

JNK (1)

Keap1-Nrf2 (1)

Ligands for Target Protein for PROTAC (1)

MEK (36)

NO Synthase (1)

p38 MAPK (2)

PARP (2)

PDGFR (2)

PDK-1 (1)

PERK (1)

PI3K (1)

Pim (1)

PKC (1)

PROTACs (1)

Raf (1)

Reference Standards (6)

SOD (1)

Topoisomerase (1)

VEGFR (3)

By Research Areas:

Cancer (43)

Cardiovascular Disease (2)

Inflammation/Immunology (8)

Metabolic Disease (3)

Neurological Disease (5)

Inhibitors & Agonists

Fluorescent Dyes

Biochemical Assay Reagents

Natural
Products

Isotope-Labeled Compounds

GMP Molecules

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-50706

Selumetinib Maximum Cited Publications 90 Publications Verification AZD6244; ARRY-142886	MEK Apoptosis	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Selumetinib (AZD6244) is selective, non-ATP-competitive oral *MEK1/2* inhibitor, with an IC₅₀ of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation. Selumetinib can penetrate the blood brain barrier (BBB) ^[1] .

HY-15202

Binimetinib 45+ Cited Publications MEK162; ARRY-162; ARRY-438162	MEK Autophagy	Cancer
Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

HY-132844

Tunlametinib HL-085	MEK	Cancer
Tunlametinib is a highly selective, orally active MEK1/2 inhibitor (IC₅₀=1.9 nM, MEK1). Tunlametinib blocks the RAS-RAF-MEK-ERK signaling pathway, arrests tumor cell cycle and promotes apoptosis. Tunlametinib potently inhibits the proliferation of RAS/RAF mutant cancer cells (such as BRAF V600E, KRAS G12C mutant cells). Tunlametinib shows synergistic anti-tumor effects with BRAF/KRASG12C/SHP2 inhibitors, Docetaxel (HY-B0011). Tunlametinib can be used to study targeted therapy for RAS/RAF mutation-driven malignancies (such as melanoma, colorectal cancer, and non-small cell lung cancer) ^[1] .

HY-147245

Basroparib STP1002	PARP	Cancer
Basroparib (STP1002) is a selective, orally active inhibitor of tankyrase (TNKS1/TNKS2) with IC₅₀ of 29.94 nM and 3.68 nM for TNKS1 and TNKS2, respectively. Basroparib has an IC₅₀ of >10 μM for PARP1. Basroparib binds to TNKS, stabilizes *AXIN1/2* proteins, blocks Wnt/β-catenin signaling pathway, inhibits tumor cell proliferation and induces apoptosis, while reducing cancer stem cell properties. Basroparib can be used in colorectal cancer (CRC) studies with KRAS mutations (such as G12V/G12D) to overcome acquired resistance to MEK inhibitors. STP1002 has synergistic antitumor activity with MEK inhibitors .

HY-12058

AZD8330 5+ Cited Publications ARRY-424704; ARRY-704	MEK	Cancer
AZD8330 (ARRY-424704) is a potent, uncompetitive *MEK1/MEK2* inhibitor, with an IC₅₀ of 7 nM.

HY-12042

Pimasertib 5+ Cited Publications AS703026; MSC1936369B	MEK	Cancer
Pimasertib (AS703026) is a highly selective, ATP non-competitive allosteric orally available *MEK1/2* inhibitor ^[1] .

HY-13425

Deguelin 10+ Cited Publications (-)-DeguelIN; (-)-cis-DeguelIN	Akt Autophagy Apoptosis	Cancer
Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.

HY-15196

TAK-285 3 Publications Verification	EGFR	Cancer
TAK-285 is a potent, selective, ATP-competitive and orally active HER2 and *EGFR(HER1)* inhibitor with IC₅₀ of 17 nM and 23 nM, respectively. TAK-285 is >10-fold selectivity for *HER1/2* than HER4, and less potent to MEK1/5, c-Met, Aurora B, Lck, CSK etc. TAK-285 has effective antitumor activity ^[1]. TAK-285 can cross the blood-brain barrier (BBB) .

HY-14691

Refametinib 10+ Cited Publications BAY 869766; RDEA119	MEK	Cancer
Refametinib (BAY 869766; RDEA119) is an orally available, potent, non-ATP-competitive, selective, allosteric *MEK1/MEK2* inhibitor with IC₅₀s of 19 nM and 47 nM, respectively.

HY-50706A

Selumetinib sulfate Maximum Cited Publications 90 Publications Verification AZD6244 sulfate; ARRY-142886 sulfate	MEK Apoptosis	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Selumetinib (AZD6244) sulfate is selective, non-ATP-competitive oral *MEK1/2* inhibitor, with an IC₅₀ of 14 nM for MEK1. Selumetinib (AZD6244) sulfate inhibits ERK1/2 phosphorylation. Selumetinib sulfate can penetrate the blood brain barrier (BBB) ^[1] .

HY-10254G

Mirdametinib 1 Publications Verification PD0325901; PD325901	MEK	Cancer
Mirdametinib (PD0325901) (GMP) is Mirdametinib (HY-10254) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Mirdametinib is an orally active, selective and non-ATP-competitive *MEK* inhibitor .

HY-B0023

Azelnidipine 3 Publications Verification CS 905	Calcium Channel MEK	Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
Azelnidipine (CS 905) is a dihydropyridine calcium channel blocker that is effective orally. Azelnidipine inhibits the intracellular calcium ion flow and lower blood pressure by selectively blocking L-type calcium channel on the membrane of vascular smooth muscle. Azelnidipine inhibits esophageal squamous cell carcinoma proliferation by targeting *MEK1/2*. Azelnidipine also has anti-inflammatory, antioxidant and neuroprotective effects ^[1] .

HY-14719

RO4987655 5+ Cited Publications CH4987655	MEK	Cancer
RO4987655 is an orally active and highly selective MEK inhibitor with an IC₅₀ of 5.2 nM for inhibition of *MEK1/MEK2*.

HY-18086

TCS PIM-1 1 4 Publications Verification SC 204330	Pim	Cancer
TCS PIM-1 1 (SC 204330) is a potent, selective and ATP-competitive *Pim-1* kianse inhibitor with an IC₅₀ of 50 nM, displays good selectivity over Pim-2 and MEK1/MEK2 (IC₅₀s >20000 nM) ^[1].

HY-12062

PD318088 1 Publications Verification	MEK	Cancer
PD318088 is a potent, allosteric and non-ATP competitive *MEK1/2* inhibitor, an analog of PD184352 (HY-50295). PD318088 binds simultaneously with ATP in a region of the MEK1 active site that is adjacent to the ATP-binding site. PD318088 can be used for cancer research ^[1].

HY-N12445

Quercetin-3'-O-glucoside 1 Publications Verification	Topoisomerase Caspase Apoptosis SOD	Metabolic Disease Inflammation/Immunology Cancer
Quercetin-3'-O-glucoside is an orally active flavonoid glycoside. Quercetin-3'-O-glucoside reduces liver glucose-6-phosphatase activity, alters serum insulin and glucose levels, and regulates the activities of antioxidant enzymes in the liver and kidney. Quercetin-3'-O-glucoside inhibits DNA topoisomerase II, induces S-phase cell cycle arrest and caspase-3-mediated apoptosis in hepatocellular carcinoma cells. Quercetin-3'-O-glucoside selectively inhibits EGFR-mediated signaling pathways targeting AKT, ERK1/2, FAK and MEK1/2. Quercetin-3'-O-glucoside inhibits growth factor-induced migration and invasion in pancreatic cancer cells. Quercetin-3'-O-glucoside exerts free radical scavenging effects. Quercetin-3'-O-glucoside is applicable to research related to pancreatic cancer, diabetes, hepatocellular carcinoma and malignant tumors ^[1] .

HY-145702

MAP855	MEK ERK	Cancer
MAP855 is a highly potent, selective, ATP-competitive and orally active *MEK1/2* kinase inhibitor (MEK1 ERK2 cascade IC₅₀=3 nM, pERK EC₅₀=5 nM). MAP855 shows equipotent inhibition of wild-type and mutant MEK1/2 ^[1].

HY-131295

PD0325901-O-C2-dioxolane 2 Publications Verification	MEK Ligands for Target Protein for PROTAC	Cancer
PD0325901-O-C2-dioxolane has main portion of MEK inhibitor PD0325901. PD0325901-O-C2-dioxolane and a ligand of VHL or CRBN E3 ligase can be used in the synthesis of MEK1/2 degrader ^[1].

HY-U00312

*MEK-IN-1*	MEK	Cancer
MEK-IN-1 is a MEK inhibitor extracted from patent WO2008076415A1.

HY-115674

ML175	Glutathione S-transferase Akt MEK	Neurological Disease Inflammation/Immunology
ML175 is a specific glutathione transferase Omega 1-1 (GSTO1-1) inhibitor. ML175 can significantly activate Akt and *MEK1/2* kinases. ML175 can be used in the research of diseases such as Parkinson's disease ^[1].

HY-113592

ERK-IN-4 1 Publications Verification	ERK	Cancer
ERK-IN-4 is an ERK inhibitor binds preferentially to ERK2 with a K_d of 5 μM. ERK-IN-4 specificity inhibits ERK Rsk-1 and Elk-1 phosphorylation. ERK-IN-4 has little effect on ERK protein phosphorylation by its upstream activator MEK1/2 ^[1].

HY-107417

Hypothemycin	VEGFR MEK FLT3 PDGFR ERK	Cancer
Hypothemycin, a fungal polyketide, is a multikinase inhibitor with K_is of 10/70 nM, 17/38 nM, 90 nM, 900 nM/1.5 μM, and 8.4/2.4 μM for *VEGFR2/VEGFR1, MEK1/MEK2, FLT-3, PDGFRβ/PDGFRα, and ERK1/ERK2*, respectively ^[1] .

HY-170982

MS910	MEK PROTACs	Cancer
MS910 is an efficient and selective MEK1/2 PROTAC degrader. MS910 exhibits effective MEK1/2 degradation ability and anti proliferative activity in various cancer cells, such as HT-29 (MEK1 DC₅₀ = 118 nM, MEK2 DC₅₀ = 55 nM) and SK-MEL-28 (MEK1 DC₅₀ = 94 nM, MEK2 DC₅₀ = 38 nM) cells. MS910 is commonly used in cancer research. (Pink: MEK1/2 Ligand (HY-10254); Blue: CRBN Ligand (HY-W087383); Black: Linker (HY-W022240)) ^[1]

HY-13425R

Deguelin (Standard) (-)-DeguelIN (Standard); (-)-cis-DeguelIN (Standard)	Akt Autophagy Apoptosis Reference Standards	Cancer
Deguelin (Standard) is the analytical standard of Deguelin. This product is intended for research and analytical applications. Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.

HY-111033

RO5068760	MEK ERK Apoptosis p38 MAPK CDK PARP	Inflammation/Immunology Cancer
RO5068760 is a potent, orally active and selective non-ATP-competitive *MEK1/2* inhibitor with an IC₅₀ of 0.025 μM for MEK1. RO5068760 significantly inhibits MAPK pathway activity, thereby inducing G1 cell cycle arrest and apoptosis to inhibit cancer cell growth. RO5068760 exhibits significant efficacy in a broad spectrum of tumors with aberrant MAPK pathway activation. RO5068760 can be used for melanoma, colorectal cancer, non-small cell lung cancer (NSCLC), and pancreatic cancer research ^[1].

HY-15202R

Binimetinib (Standard) MEK162 (Standard); ARRY-162 (Standard); ARRY-438162 (Standard)	Reference Standards MEK Autophagy	Cancer
Binimetinib (Standard) is the analytical standard of Binimetinib. This product is intended for research and analytical applications. Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

HY-50706R

Selumetinib (Standard) AZD6244 (Standard); ARRY-142886 (Standard)	MEK Apoptosis Reference Standards	Cancer
Selumetinib (Standard) is the analytical standard of Selumetinib. This product is intended for research and analytical applications. Selumetinib (AZD6244) is selective, non-ATP-competitive oral MEK1/2 inhibitor, with an IC50 of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation.

HY-181067

IK-595	MEK ERK	Cancer
IK-595 is a MEK1/MEK2 inhibitor with high affinity (7.39 nM).IK-595 blocks EGF-induced ERK1/2 phosphorylation in AsPC-1 cells with IC₅₀ value of 0.1 nM. IK-595 has oral activity and blood-brain barrier penetration. IK-595 can be used for the research of Ras/MAPK pathway-altered cancers ^[1].

HY-12482

X-370	PI3K Apoptosis PDK-1 MEK Akt ERK	Cancer
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) ^[1].

HY-10338A

Foretinib phosphate	c-Met/HGFR VEGFR	Cancer
Foretinib phosphate is an orally bioavailable small molecule with potential anti-tumor activity. Foretinib phosphate can selectively inhibit hepatocyte growth factor (HGF) receptor c-MET and vascular endothelial growth factor receptor 2 (VEGFR2), thereby potentially inhibiting tumor angiogenesis, tumor cell proliferation and metastasis. Foretinib phosphate shows different anti-cancer activity from cabozantinib in lung cancer cells and has stronger inhibitory effects on targets such as MEK1/2, FER and AURKB ^[1].

HY-123586

L-783277	MEK VEGFR FLT3 PDGFR	Cancer
L-783277 (Compound 4) is a MEK inhibitor (IC₅₀ = 4 nM). L-783277 has potent inhibitory activity against a variety of kinases, including VEGFR2/3, *FLT1/3/4, MEK1/2, KDR, and PDGFRα, but has low selectivity for the kinase community. L-783277 inhibits viability (IC₅₀* = 22 mM) and cell proliferation (IC₅₀ = 21 mM) of H295R cells. L-783277 could be used in research on cancers such as adrenocortical carcinoma ^[1] .

HY-145701

MEK1/2-IN-2	MEK	Cancer
MEK1/2-IN-2 is a potent ATP-competitive *MEK1/2* inhibitor and shows equipotent inhibition of WT MEK1/2 and a panel of MEK1/2 mutant cell lines ^[1].

HY-12447

SMK-17	MEK Apoptosis	Cancer
SMK-17 is a selective, non-ATP-competitive *MEK1/MEK2* inhibitor with IC₅₀s of 62 nM and 56 nM, respectively. SMK-17 binds to the allosteric pocket of MEK1/2. SMK-17 induces apoptosis in tumor cell lines harboring β-catenin mutations ^[1].

HY-12042A

Pimasertib hydrochloride AS703026 hydrochloride; MSC1936369B hydrochloride	MEK	Cancer
Pimasertib hydrochloride is a highly selective, ATP non-competitive allosteric orally available *MEK1/2* inhibitor ^[1] .

HY-50295A

CI-1040 hydrochloride PD 184352 hydrochloride	MEK Apoptosis	Cancer
CI-1040 (PD 184352) hydrochloride is an orally active, highly specific inhibitor of MEK, with an IC₅₀ of 17 nM for *MEK1* .

HY-13303

RO 4927350	MEK	Cancer
RO 4927350 is a potent and selective non-ATP-competitive MEK1/2 inhibitor. RO 4927350 exhibits significant antitumor efficacy in a broad spectrum of tumor models ^[1].

HY-126048

JTP-70902	MEK	Cancer
JTP-70902, a p15 ^INK4b-inductive compound, is a *MEK1/2* inhibitor. JTP-70902 exhibits potent antitumor effect ^[1].

HY-14719R

RO4987655 (Standard) CH4987655 (Standard)	MEK Reference Standards	Cancer
RO4987655 (Standard) is the analytical standard of RO4987655. This product is intended for research and analytical applications. RO4987655 is an orally active and highly selective MEK inhibitor with an IC50 of 5.2 nM for inhibition of MEK1/MEK2.

HY-15202S3

Binimetinib-d4 MEK162-d₄; ARRY-162-d₄; ARRY-438162-d₄	Isotope-Labeled Compounds Autophagy MEK	Cancer
Binimetinib-d₄ (MEK162-d₄) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

HY-15202S1

Binimetinib-d3 MEK162-d₃; ARRY-162-d₃; ARRY-438162-d₃	Isotope-Labeled Compounds MEK Autophagy	Cancer
Binimetinib-d₃ (MEK162-d₃) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM ^[1].

HY-14691R

Refametinib (Standard) BAY 869766 (Standard); RDEA119 (Standard)	MEK Reference Standards	Cancer
Refametinib (Standard) is the analytical standard of Refametinib. This product is intended for research and analytical applications. Refametinib (BAY 869766; RDEA119) is an orally available, potent, non-ATP-competitive, selective, allosteric MEK1/MEK2 inhibitor with IC50s of 19 nM and 47 nM, respectively.

HY-50706AR

Selumetinib sulfate (Standard) AZD6244 sulfate (Standard); ARRY-142886 sulfate (Standard)	MEK Apoptosis Reference Standards	Cancer
Selumetinib (sulfate) (Standard) is the analytical standard of Selumetinib (sulfate). This product is intended for research and analytical applications. Selumetinib (AZD6244) is selective, non-ATP-competitive oral MEK1/2 inhibitor, with an IC50 of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation.

HY-130642

(S,R,S)-AHPC-Me-C10-Br	E3 Ligase Ligand-Linker Conjugates	Cancer
(S,R,S)-AHPC-Me-C10-Br is a synthesized E3 ligase ligand-linker conjugate. (S,R,S)-AHPC-Me-C10-Br incorporates a VHL E3 ligase linker and MS432 based on the MEK1/2 inhibitor PD0325901 ^[1].

HY-120485

Raxofelast IRFI-016	p38 MAPK ERK PKC	Cardiovascular Disease
Raxofelast (IRFI-016) is an antioxidant agent in various models of ischemia-reperfusion injury. Raxofelast has antiproliferative activity in H₂O₂-stimulated rat aortic smooth muscle cells. Raxofelast attenuates the activation of mitogen-activating protein kinase (MAPK), ERK kinase 1, 2 (MEK1,2) and protein kinase C (PKC) without affecting Ras expression ^[1].

HY-173153

BRAFV600E/JNK-IN-1	JNK PERK MEK NO Synthase	Inflammation/Immunology Cancer
BRAFV600E/JNK-IN-1 (Compound 14c) is an inhibitor of JNK1, JNK2, JNK3 and BRAFV600E, with IC₅₀ values of 0.51 μM, 0.53 μM, 1.02 μM and 0.009 μM, respectively. BRAFV600E/JNK-IN-1 can inhibit the phosphorylation of *MEK1/2* and *ERK1/2. In addition, BRAFV600E/JNK-IN-1 can inhibit tumor cell proliferation, NO release and PGE2* production, and has anti-tumor and anti-inflammatory activities ^[1].

HY-180327

NEPP11	Drug Derivative Apoptosis Keap1-Nrf2 Raf MEK ERK	Neurological Disease Inflammation/Immunology
NEPP11 is a cyclopentenone prostaglandin analogue. NEPP11 can inhibit glutamate-induced HT22 cell death in mouse hippocampus and prevent manganese-induced apoptosis in PC12 cells. NEPP11 can activate Nrf2 and maintain *MEK1/2* and *ERK1/2* activity by inhibiting c-Raf downregulation. NEPP11 exerts a neuroprotective effect in a mouse model of focal cerebral ischemia caused by permanent middle cerebral artery occlusion ^[1].

Cat. No.	Product Name	Type

HY-10254G

Mirdametinib 1 Publications Verification PD0325901; PD325901	Fluorescent Dyes
Mirdametinib (PD0325901) (GMP) is Mirdametinib (HY-10254) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Mirdametinib is an orally active, selective and non-ATP-competitive *MEK* inhibitor .

Cat. No.	Product Name	Type

HY-10254G

Mirdametinib 1 Publications Verification PD0325901; PD325901	Biochemical Assay Reagents
Mirdametinib (PD0325901) (GMP) is Mirdametinib (HY-10254) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Mirdametinib is an orally active, selective and non-ATP-competitive *MEK* inhibitor .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-13425

Deguelin 10+ Cited Publications (-)-DeguelIN; (-)-cis-DeguelIN	Flavonoids Classification of Application Fields Leguminosae Isoflavanones Derris trifoliata Lour. Plants Disease Research Fields Biological Pesticide Research Source Classification Cancer Agricultural Research	Akt Autophagy Apoptosis
Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.

HY-N12445

Quercetin-3'-O-glucoside 1 Publications Verification	Malvaceae Structural Classification Flavonols Flavonoids Abelmoschus manihot (Linn.) Medicus Plants Source Classification	Topoisomerase Caspase Apoptosis SOD
Quercetin-3'-O-glucoside is an orally active flavonoid glycoside. Quercetin-3'-O-glucoside reduces liver glucose-6-phosphatase activity, alters serum insulin and glucose levels, and regulates the activities of antioxidant enzymes in the liver and kidney. Quercetin-3'-O-glucoside inhibits DNA topoisomerase II, induces S-phase cell cycle arrest and caspase-3-mediated apoptosis in hepatocellular carcinoma cells. Quercetin-3'-O-glucoside selectively inhibits EGFR-mediated signaling pathways targeting AKT, ERK1/2, FAK and MEK1/2. Quercetin-3'-O-glucoside inhibits growth factor-induced migration and invasion in pancreatic cancer cells. Quercetin-3'-O-glucoside exerts free radical scavenging effects. Quercetin-3'-O-glucoside is applicable to research related to pancreatic cancer, diabetes, hepatocellular carcinoma and malignant tumors ^[1] .

HY-107417

Hypothemycin	Monophenols Microorganisms Antifungal Macrolide Antibiotics Classification of Application Fields Antibiotics Phenols Disease Research Disease Research Fields Source Classification Cancer	VEGFR MEK FLT3 PDGFR ERK
Hypothemycin, a fungal polyketide, is a multikinase inhibitor with K_is of 10/70 nM, 17/38 nM, 90 nM, 900 nM/1.5 μM, and 8.4/2.4 μM for *VEGFR2/VEGFR1, MEK1/MEK2, FLT-3, PDGFRβ/PDGFRα, and ERK1/ERK2*, respectively ^[1] .

HY-13425R

Deguelin (Standard) (-)-DeguelIN (Standard); (-)-cis-DeguelIN (Standard)	Structural Classification Flavonoids Leguminosae Isoflavanones Derris trifoliata Lour. Plants Source Classification	Akt Autophagy Apoptosis Reference Standards
Deguelin (Standard) is the analytical standard of Deguelin. This product is intended for research and analytical applications. Deguelin, a naturally occurring rotenoid, acts as a chemopreventive agent by blocking multiple pathways like PI3K-Akt, IKK-NF-κB, and MAPK-mTOR-survivin-mediated apoptosis. Deguelin binding to Hsp90 leads to a decreased expression of numerous oncogenic proteins, including MEK1/2, Akt, HIF1α, COX-2, and NF-κB.

Cat. No.	Product Name	Chemical Structure

HY-15202S3

Binimetinib-d4
Binimetinib-d₄ (MEK162-d₄) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM.

HY-15202S1

Binimetinib-d3
Binimetinib-d₃ (MEK162-d₃) is deuterium labeled Binimetinib. Binimetinib (MEK162) is an oral and selective *MEK1/2* inhibitor. Binimetinib (MEK162) inhibits MEK with an IC₅₀ of 12 nM ^[1].

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-10254G

Mirdametinib 1 Publications Verification PD0325901; PD325901	MEK	Cancer
Mirdametinib (PD0325901) (GMP) is Mirdametinib (HY-10254) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Mirdametinib is an orally active, selective and non-ATP-competitive *MEK* inhibitor .

Inquiry Online

Your information is safe with us. * Required Fields.

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社重松貿易株式会社
Salutation			Country or Region *
Applicant Name *			Organization Name *
Department *
Email Address *			Product Name *
Cat. No.			Requested quantity *
Phone Number *
Remarks

Inquiry Online

Inquiry Information

Product Name:
Cat. No.:
Quantity:
MCE Japan Authorized Agent:

MEK-IN-1

Inhibitors & Agonists

Fluorescent Dyes

Biochemical Assay Reagents

NaturalProducts

Isotope-Labeled Compounds

GMP Molecules

Natural
Products