Search Result

Pathways Recommended:	MAPK/ERK Pathway Neuronal Signaling JAK/STAT Signaling

Results for "

MAPK/ERK signaling axis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	ERK (4) p38 MAPK (4) Akt (4) Apoptosis (4) Bcl-2 Family (1) c-Myc (1) CXCR (1) Environmental Pollutants (2) FOXO (1) Indoleamine 2,3-Dioxygenase (IDO) (2) Isotope-Labeled Compounds (1) JNK (3) Mitophagy (2) Monoamine Oxidase (2) NF-κB (2) PERK (1) PI3K (3) PPAR (2) Reactive Oxygen Species (ROS) (2)
By Research Areas:	Cancer (3) Cardiovascular Disease (2) Endocrinology (2) Inflammation/Immunology (2) Metabolic Disease (2) Neurological Disease (2)

Inhibitors & Agonists

Inhibitory Antibodies

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: RGS Protein ERK p38 MAPK MAP4K MAPKAPK2 (MK2) MNK

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-N0863

Methyl protodioscin NSC-698790; Smilax saponin B	Bcl-2 Family Apoptosis Akt c-Myc ERK p38 MAPK JNK FOXO	Cancer
Methyl protodioscin (NSC-698790; Smilax saponin B) is a multi-target, selective, steroidal diglycoside inhibitor with antitumor activity that induces cell cycle arrest. The mechanism of action of Methyl protodioscin is complex, involving the induction of G2/M cell cycle arrest, regulation of the Bcl-2/Bax apoptotic pathway, inhibition of the Akt1/c-Myc axis and *MAPK/ERK* signaling, while simultaneously downregulating ADAM15 and inducing FOXO1 to reduce cholesterol synthesis. It also inhibits the JNK/c-Jun pathway, reducing the production of inflammatory factors (IL-6, TNF-α). Methyl protodioscin exhibits significant antitumor (inhibiting proliferation, migration, invasion, and inducing apoptosis), anti-inflammatory, and anti-restenosis activities. Methyl protodioscin can be used in research on lung cancer, prostate cancer, pancreatic cancer, and other tumors, as well as inflammatory diseases such as airway inflammation and enteritis .

HY-Y1322

Triphenyl phosphate	Environmental Pollutants Mitophagy Apoptosis NF-κB p38 MAPK ERK JNK PI3K Akt Monoamine Oxidase Reactive Oxygen Species (ROS) PPAR Indoleamine 2,3-Dioxygenase (IDO)	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the *MAPK/ERK* pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring .

HY-Y1322S

Triphenyl phosphate-d15 Celluflex TPP-d₁₅; DHPF 005-d₁₅; Disflamol TP-d₁₅; Disflamoll TP-d₁₅; NSC 57868-d₁₅; Phenyl phosphate ((PhO)3PO)-d₁₅; Phoscon FR 903N-d₁₅	Isotope-Labeled Compounds Environmental Pollutants ERK Indoleamine 2,3-Dioxygenase (IDO) p38 MAPK NF-κB Akt Monoamine Oxidase Mitophagy Reactive Oxygen Species (ROS) JNK PI3K PPAR Apoptosis	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
Triphenyl phosphate-d₁₅ is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the *MAPK/ERK* pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

HY-183316

Anticancer agent 319	Akt PI3K PERK p38 MAPK ERK Apoptosis	Cancer
Anticancer agent 319 is an anticancer agent. Anticancer agent 319 inhibits the proliferation of liver cancer cells. Anticancer agent 319 inhibits AKT phosphorylation and blocks the PI3K/AKT signaling axis; meanwhile, it inhibits *ERK1/2* phosphorylation and blocks the *MAPK/ERK* signaling axis. Anticancer agent 319 induces G2/M phase cell cycle arrest, triggers apoptosis, and reduces mitochondrial membrane potential in liver cancer cells. Anticancer agent 319 can be used for the research of hepatocellular carcinoma .

HY-P991744

Anti-Mouse CXCR4 Antibody (Cx4Mab-1)	CXCR	Cancer
Anti-Mouse CXCR4 Antibody is a monoclonal antibody that specifically recognizes murine CXCR4 (C-X-C chemokine receptor 4), also known as fusin or CD184. CXCR4 is a seven-transmembrane G protein–coupled receptor whose principal endogenous ligand is CXCL12 (stromal cell–derived factor-1α, SDF-1α) and is widely expressed in hematopoietic cells, endothelial cells, neurons, as well as embryonic and adult stem cells. The CXCR4–CXCL12 signaling axis activates multiple downstream pathways, including ERK1/2, Ras, p38 MAPK, PLC/MAPK, and SAPK/JNK, thereby regulating cell survival, proliferation, migration, and stemness maintenance. Aberrant overexpression of CXCR4 is closely associated with poor prognosis and metastasis in various cancers, with CXCR4-positive tumor cells preferentially home to CXCL12-rich tissues such as the liver, bone marrow, lung, and lymph nodes. Accordingly, CXCR4 and its CXCL12-related antagonists emerge as attractive targets for experimental anticancer therapy. Anti-Mouse CXCR4 Antibody is generated using a cell-based immunization and screening strategy and exhibits high affinity for both endogenous and exogenous murine CXCR4. Anti-Mouse CXCR4 Antibody can be used for thestudy of chronic lymphocytic leukemia and multiple myeloma .

Cat. No.	Product Name	Target	Research Area	Image

HY-P991744

Anti-Mouse CXCR4 Antibody (Cx4Mab-1)	CXCR	Cancer
Anti-Mouse CXCR4 Antibody is a monoclonal antibody that specifically recognizes murine CXCR4 (C-X-C chemokine receptor 4), also known as fusin or CD184. CXCR4 is a seven-transmembrane G protein–coupled receptor whose principal endogenous ligand is CXCL12 (stromal cell–derived factor-1α, SDF-1α) and is widely expressed in hematopoietic cells, endothelial cells, neurons, as well as embryonic and adult stem cells. The CXCR4–CXCL12 signaling axis activates multiple downstream pathways, including ERK1/2, Ras, p38 MAPK, PLC/MAPK, and SAPK/JNK, thereby regulating cell survival, proliferation, migration, and stemness maintenance. Aberrant overexpression of CXCR4 is closely associated with poor prognosis and metastasis in various cancers, with CXCR4-positive tumor cells preferentially home to CXCL12-rich tissues such as the liver, bone marrow, lung, and lymph nodes. Accordingly, CXCR4 and its CXCL12-related antagonists emerge as attractive targets for experimental anticancer therapy. Anti-Mouse CXCR4 Antibody is generated using a cell-based immunization and screening strategy and exhibits high affinity for both endogenous and exogenous murine CXCR4. Anti-Mouse CXCR4 Antibody can be used for thestudy of chronic lymphocytic leukemia and multiple myeloma .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N0863

Methyl protodioscin NSC-698790; Smilax saponin B	Structural Classification other families Classification of Application Fields Plants Disease Research Fields Steroids Source Classification Cancer	Bcl-2 Family Apoptosis Akt c-Myc ERK p38 MAPK JNK FOXO
Methyl protodioscin (NSC-698790; Smilax saponin B) is a multi-target, selective, steroidal diglycoside inhibitor with antitumor activity that induces cell cycle arrest. The mechanism of action of Methyl protodioscin is complex, involving the induction of G2/M cell cycle arrest, regulation of the Bcl-2/Bax apoptotic pathway, inhibition of the Akt1/c-Myc axis and *MAPK/ERK* signaling, while simultaneously downregulating ADAM15 and inducing FOXO1 to reduce cholesterol synthesis. It also inhibits the JNK/c-Jun pathway, reducing the production of inflammatory factors (IL-6, TNF-α). Methyl protodioscin exhibits significant antitumor (inhibiting proliferation, migration, invasion, and inducing apoptosis), anti-inflammatory, and anti-restenosis activities. Methyl protodioscin can be used in research on lung cancer, prostate cancer, pancreatic cancer, and other tumors, as well as inflammatory diseases such as airway inflammation and enteritis .

Cat. No.	Product Name	Chemical Structure

HY-Y1322S

Triphenyl phosphate-d15
Triphenyl phosphate-d₁₅ is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the *MAPK/ERK* pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

Triphenyl phosphate-d15

Triphenyl phosphate-d₁₅ is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

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