500

U0126

500 Publications Verification

Cat. No.: HY-12031A

CAS No.: 109511-58-2

Purity: 98.57%

Target:

MEK Autophagy Mitophagy Influenza Virus

Research Areas:

Cancer

U0126 is a potent, non-ATP competitive and selective MEK1 and MEK2 inhibitor, with IC₅₀s of 72 nM and 58 nM, respectively. U0126 is an autophagy and mitophagy inhibitor ^[1] .

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500

U0126-EtOH

500 Publications Verification

Cat. No.: HY-12031

CAS No.: 1173097-76-1

Purity: 98.92%

Target:

MEK Autophagy Mitophagy Influenza Virus

Research Areas:

Cancer

U0126 (U0126-EtOH) is a potent, non-ATP competitive and selective MEK1 and MEK2 inhibitor, with IC₅₀s of 72 nM and 58 nM, respectively. U0126 is an autophagy and mitophagy inhibitor ^[1] .

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434

PD98059

434 Cited Publications

Cat. No.: HY-12028

CAS No.: 167869-21-8

Purity: 98.89%

Target:

MEK ERK Aryl Hydrocarbon Receptor Autophagy

Research Areas:

Cancer

PD98059 is a potent and selective MEK inhibitor with an IC₅₀ of 5 µM. PD98059 binds to the inactive form of MEK, thereby preventing the activation of MEK1 (IC₅₀ of 2-7 µM) and MEK2 (IC₅₀ of 50 µM) by upstream kinases. PD98059 is a ERK1/2 signaling inhibitor. PD98059 is a ligand for the aryl hydrocarbon receptor (AHR), and suppresses TCDD binding (IC₅₀ of 4 μM) and AHR transformation (IC₅₀ of 1 μM). PD98059 also inhibits Mycobacterium bovis Bacillus CalmetteGuerin (BCG)-induced autophagy ^[1] .

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318

Trametinib

318 Cited Publications

Cat. No.: HY-10999

CAS No.: 871700-17-3

Purity: 99.93%

Synonyms: GSK1120212; JTP-74057

Target:

MEK Autophagy Apoptosis

Research Areas:

Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer

Trametinib (GSK1120212; JTP-74057) is an orally active MEK inhibitor that inhibits MEK1 and MEK2 with IC₅₀s of about 2 nM. Trametinib activates autophagy and induces apoptosis, cross the blood-brain barrier (BBB), used in research related to subarachnoid hemorrhage (SAH) ^[1] .

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318

Trametinib (DMSO solvate)

318 Cited Publications

Cat. No.: HY-10999A

CAS No.: 1187431-43-1

Purity: 99.56%

Synonyms: GSK-1120212 (DMSO solvate); JTP-74057 (DMSO solvate)

Target:

MEK Apoptosis

Research Areas:

Cancer

Trametinib (DMSO solvate) (GSK-1120212 (DMSO solvate)) is an orally active MEK inhibitor that inhibits MEK1 and MEK2 with IC₅₀s of about 2 nM. Trametinib (DMSO solvate) activates autophagy and induces apoptosis ^[1] . This product is in solid form, a DMSO solvate, and a stable crystalline form.

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163

Mirdametinib

163 Cited Publications

Cat. No.: HY-10254

CAS No.: 391210-10-9

Purity: 99.95%

Synonyms: PD0325901; PD325901

Target:

MEK Autophagy Apoptosis

Research Areas:

Cancer

Mirdametinib (PD0325901) is an orally active, selective and non-ATP-competitive MEK inhibitor with an IC₅₀ of 0.33 nM. Mirdametinib exhibits a K_i ^app of 1 nM against activated MEK1 and MEK2. Mirdametinib suppresses the expression of p-ERK1/2 and induces apoptosis. Mirdametinib has anti-cancer activity for a broad spectrum of human tumor xenografts ^[1] .

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103

Selumetinib

103 Cited Publications

Cat. No.: HY-50706

CAS No.: 606143-52-6

Synonyms: AZD6244; ARRY-142886

Target:

MEK Apoptosis

Research Areas:

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] .

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103

Selumetinib sulfate

103 Cited Publications

Cat. No.: HY-50706A

CAS No.: 943332-08-9

Synonyms: AZD6244 sulfate; ARRY-142886 sulfate

Target:

MEK Apoptosis

Research Areas:

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] .

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63

Cobimetinib

63 Cited Publications

Cat. No.: HY-13064

CAS No.: 934660-93-2

Purity: 99.81%

Synonyms: GDC-0973; XL518

Target:

MEK Apoptosis

Research Areas:

Cancer

Cobimetinib (GDC-0973, RG7420) is a potent, selective and oral MEK1 inhibitor with an IC₅₀ of 4.2 nM for MEK1.

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63

Cobimetinib hemifumarate

63 Cited Publications

Cat. No.: HY-13064A

CAS No.: 1369665-02-0

Purity: 99.73%

Synonyms: GDC-0973 hemifumarate; XL-518 hemifumarate

Target:

MEK Apoptosis

Research Areas:

Cancer

Cobimetinib hemifumarate is a novel selective MEK1 inhibitor, and the IC₅₀ value against MEK1 is 4.2 nM.

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56

Binimetinib

56 Cited Publications

Cat. No.: HY-15202

CAS No.: 606143-89-9

Purity: 99.31%

Synonyms: MEK162; ARRY-162; ARRY-438162

Target:

MEK Autophagy

Research Areas:

Cancer

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

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52

Idasanutlin

52 Cited Publications

Cat. No.: HY-15676

CAS No.: 1229705-06-9

Purity: 99.93%

Synonyms: RG7388

Target:

MDM-2/p53 E1/E2/E3 Enzyme Apoptosis Pyroptosis Reactive Oxygen Species (ROS) Caspase

Research Areas:

Neurological Disease Cancer

Idasanutlin (RG7388) is an orally bioavailable MDM2 inhibitor with an IC₅₀ of 6 nM. Idasanutlin disrupts MDM2-p53 binding, stabilizes and activates p53, triggering cell cycle arrest, apoptosis, and reduced cancer cell viability. Idasanutlin reduces EGFR protein expression and phosphorylation, suppresses downstream SHP2, MEK1/2, ERK1/2, AKT, mTOR, p70(S6K1), and S6 signaling. Idasanutlin induces mitochondrial ROS production, drives p38 MAPK phosphorylation, upregulates NOXA, and mediates caspase-3-dependent apoptosis and gasdermin E-mediated pyroptosis. Idasanutlin can be used for the research of TP53-mutant non-small cell lung cancer, T-cell acute lymphoblastic leukemia, colorectal carcinoma, melanoma, diffuse large B-cell lymphoma, mantle cell lymphoma, non-Hodgkin lymphoma, severe fever with thrombocytopenia syndrome, neuroblastoma, acute lymphoblastic leukemia, relapsed or refractory acute myeloid leukemia, osteosarcoma, solid tumors, and hematological tumors ^[1] .

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