JAK1/STAT6 signaling pathway

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

By Targets:	JAK (7) STAT (7) Akt (5) AMPK (5) Apoptosis (5) Endogenous Metabolite (5) Ferroptosis (5) Interleukin Related (6) JNK (5) NF-κB (5) p38 MAPK (5) PI3K (5) Reference Standards (2) Sirtuin (5) TNF Receptor (6)
By Research Areas:	Cardiovascular Disease (4) Inflammation/Immunology (7) Metabolic Disease (1) Neurological Disease (4)

Targets Recommended: STAT Tissue Factor Pathway Inhibitor (TFPI) JAK RGS Protein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-113402

Gamma-glutamylcysteine 4 Publications Verification γ-Glu-Cys	Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-125019

iJak-381	JAK STAT	Inflammation/Immunology
iJak-381 is a *JAK1/2* inhibitor with anti-inflammatory activity. iJak-381 blocks IL-13 signaling and also inhibits IL-4 and IL-6 signaling pathways. iJak-381 also reduced p-STAT6 levels and inhibited the influx of inflammatory cells into the lungs of mice. iJak-381 inhibits airway hyperresponsiveness (AHR) .

HY-113402R

Gamma-glutamylcysteine (Standard) γ-Glu-Cys (Standard)	Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Inflammation/Immunology
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

HY-113402AR

Gamma-glutamylcysteine TFA (Standard) γ-Glu-Cys TFA (Standard)	Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

HY-123115

Leucrose 5-O-α-D-Glucopyranosyl-D-fructose	JAK STAT TNF Receptor Interleukin Related	Metabolic Disease Inflammation/Immunology
Leucrose (5-O-α-D-Glucopyranosyl-D-fructose) is an orally active Sucrose (HY-B1779) isomer naturally found in pollen and honey. Leucrose promotes phosphorylation of JAK1 and STAT6, reduces pro-inflammatory mediators and cytokinesas (TNFα, and IL-1β), increases M2 macrophage polarization and suppresses DSS (HY-116282C)-induced colitis. Leucrose suppresses hepatic triglyceride accumulation, improves fasting blood glucose levels, and regulates hepatic lipogenesis and fatty acid β-oxidation in high-fat diet-induced obese mice. Leucrose is slowly hydrolyzed into glucose and fructose by α-glucosidase and acts as as a sugar substitute in diet .

HY-113402B

Gamma-glutamylcysteine ammonium γ-Glu-Cys ammonium	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

Cat. No.	Product Name

HY-L008

JAK/STAT Compound Library	709 compounds
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specific cytokines, and is critical in blood formation and immune response. Canonical JAK/STAT signaling begins with the association of cytokines and their corresponding transmembrane receptors. Activated JAKs then phosphorylate latent STAT monomers, leading to dimerization, nuclear translocation, and DNA binding. In mammals, there are four JAKs (JAK1, JAK2, JAK3, TYK2) and seven STATs (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, STAT6). Since the JAK/STAT pathway plays a major role in many fundamental processes, such as apoptosis and inflammation, dysfunctional proteins in the pathway may lead to a number of diseases. For example, alterations in JAK/STAT signalling can result in cancer and diseases affecting the immune system, such as severe combined immunodeficiency disorder (SCID). MCE provides 709 compounds that can be used in the study of the JAK/STAT signaling pathway and related diseases.

JAK/STAT Compound Library

709 compounds

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specific cytokines, and is critical in blood formation and immune response. Canonical JAK/STAT signaling begins with the association of cytokines and their corresponding transmembrane receptors. Activated JAKs then phosphorylate latent STAT monomers, leading to dimerization, nuclear translocation, and DNA binding. In mammals, there are four JAKs (JAK1, JAK2, JAK3, TYK2) and seven STATs (STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b, STAT6). Since the JAK/STAT pathway plays a major role in many fundamental processes, such as apoptosis and inflammation, dysfunctional proteins in the pathway may lead to a number of diseases. For example, alterations in JAK/STAT signalling can result in cancer and diseases affecting the immune system, such as severe combined immunodeficiency disorder (SCID).

MCE provides 709 compounds that can be used in the study of the JAK/STAT signaling pathway and related diseases.

Cat. No.	Product Name	Type

HY-123115

Leucrose 5-O-α-D-Glucopyranosyl-D-fructose	Biochemical Assay Reagents
Leucrose (5-O-α-D-Glucopyranosyl-D-fructose) is an orally active Sucrose (HY-B1779) isomer naturally found in pollen and honey. Leucrose promotes phosphorylation of JAK1 and STAT6, reduces pro-inflammatory mediators and cytokinesas (TNFα, and IL-1β), increases M2 macrophage polarization and suppresses DSS (HY-116282C)-induced colitis. Leucrose suppresses hepatic triglyceride accumulation, improves fasting blood glucose levels, and regulates hepatic lipogenesis and fatty acid β-oxidation in high-fat diet-induced obese mice. Leucrose is slowly hydrolyzed into glucose and fructose by α-glucosidase and acts as as a sugar substitute in diet .

Leucrose

5-O-α-D-Glucopyranosyl-D-fructose

Biochemical Assay Reagents

Leucrose (5-O-α-D-Glucopyranosyl-D-fructose) is an orally active Sucrose (HY-B1779) isomer naturally found in pollen and honey. Leucrose promotes phosphorylation of JAK1 and STAT6, reduces pro-inflammatory mediators and cytokinesas (TNFα, and IL-1β), increases M2 macrophage polarization and suppresses DSS (HY-116282C)-induced colitis. Leucrose suppresses hepatic triglyceride accumulation, improves fasting blood glucose levels, and regulates hepatic lipogenesis and fatty acid β-oxidation in high-fat diet-induced obese mice. Leucrose is slowly hydrolyzed into glucose and fructose by α-glucosidase and acts as as a sugar substitute in diet .

Cat. No.	Product Name	Target	Research Area

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-113402

Gamma-glutamylcysteine 4 Publications Verification γ-Glu-Cys	Structural Classification Human Gut Microbiota Metabolites Microorganisms Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Structural Classification Natural Products Classification of Application Fields Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .

HY-113402R

Gamma-glutamylcysteine (Standard) γ-Glu-Cys (Standard)	Structural Classification Human Gut Microbiota Metabolites Microorganisms Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

HY-113402AR

Gamma-glutamylcysteine TFA (Standard) γ-Glu-Cys TFA (Standard)	Structural Classification Natural Products Endogenous metabolite Source Classification	Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, *IL-4/STAT6*, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, *JAK1/STAT1*/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

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

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Peptides

Natural
Products

Name
Email *

	Sorry, but the email address you supplied was invalid.

JAK1/STAT6 signaling pathway

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Peptides

NaturalProducts

Natural
Products