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Results for "

M2 marker

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (3) Apoptosis (6) Atg8/LC3 (1) Autophagy (1) c-Myc (1) Cathepsin (1) CCR (2) CDK (2) DNA/RNA Synthesis (2) EGFR (1) Epigenetic Reader Domain (1) ERK (1) Ferroptosis (1) Indoleamine 2,3-Dioxygenase (IDO) (2) Interleukin Related (1) LDLR (2) Microtubule/Tubulin (2) Mitochondrial Metabolism (2) NF-κB (2) Opioid Receptor (1) p38 MAPK (2) p62 (1) PARP (1) PI3K (3) PROTACs (1) Reactive Oxygen Species (ROS) (3) Reference Standards (1) ROCK (2) Sigma Receptor (1) STAT (2) TNF Receptor (2) VEGFR (2)
By Research Areas:	Cancer (8) Cardiovascular Disease (2) Inflammation/Immunology (5) Metabolic Disease (2) Neurological Disease (4)

By Targets:

Akt (3)

Apoptosis (6)

Atg8/LC3 (1)

Autophagy (1)

c-Myc (1)

Cathepsin (1)

CCR (2)

CDK (2)

DNA/RNA Synthesis (2)

EGFR (1)

Epigenetic Reader Domain (1)

ERK (1)

Ferroptosis (1)

Indoleamine 2,3-Dioxygenase (IDO) (2)

Interleukin Related (1)

LDLR (2)

Microtubule/Tubulin (2)

Mitochondrial Metabolism (2)

NF-κB (2)

Opioid Receptor (1)

p38 MAPK (2)

p62 (1)

PARP (1)

PI3K (3)

PROTACs (1)

Reactive Oxygen Species (ROS) (3)

Reference Standards (1)

ROCK (2)

Sigma Receptor (1)

STAT (2)

TNF Receptor (2)

VEGFR (2)

By Research Areas:

Cancer (8)

Cardiovascular Disease (2)

Inflammation/Immunology (5)

Metabolic Disease (2)

Neurological Disease (4)

Inhibitors & Agonists

Peptides

Natural
Products

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-B1076

Medrysone 1 Publications Verification HMS; 6α-Methyl-11β-hydroxyprogesterone	VEGFR CCR STAT	Neurological Disease
Medrysone (HMS; 6α-Methyl-11β-hydroxyprogesterone) is a STAT6 modulator and M2 macrophage polarization inducer. Medrysone enhances IL-4-triggered STAT6 activation, upregulates the expression of M2 markers, and promotes the secretion of VEGF and CCL2. Medrysone also enhances the pro-migratory activity of M2-like macrophages toward endothelial cells. By regulating macrophage polarization and related repair pathways, Medrysone significantly promotes corneal wound repair in a rat mechanical injury model. Medrysone can be used for research related to corneal injury .

HY-N0430

Coptisine Coptisin	Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .

HY-N0430A

Coptisine Sulfate 5 Publications Verification	Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .

HY-118762

KGP94	Cathepsin	Cancer
KGP94 is a selective inhibitor of cathepsin L with an IC₅₀ of 189 nM . KGP94 inhibits migration and invasion of metastatic carcinoma and shows low cytotoxicity (GI₅₀=26.9 µM) against various human cell lines .

HY-P11107

RP-832c	Apoptosis TNF Receptor	Inflammation/Immunology Cancer
RP-832c is a synthetic analogue of host defense peptides (HDP), targeting the mannose receptor CD206 on the surface of M2 polarized macrophages (K_d = 3.5 μM). RP-832c binding to CD206 induces a significant conformational change in the receptor, activating signaling pathways that lead to rapid apoptosis and repolarization of CD206-positive M2 macrophages to an M1 phenotype. RP-832c treatment significantly reduces CD206 gene expression in M2 macrophages while transiently increasing expression of TNF-α, a marker for M1 macrophages. RP-832c is used for the studies of T-cell lymphoma (CTCL) and idiopathic pulmonary fibrosis (IPF) .

HY-178945

KOR agonist 7	Opioid Receptor Interleukin Related TNF Receptor Sigma Receptor	Neurological Disease Inflammation/Immunology
KOR agonist 7 (Compound 29) is a highly selective κ-opioid receptor (KOR) agonist with a K_i of 138 nM. KOR agonist 7 shows no activity at μ- and δ-opioid receptors or σ1 receptor, and exhibits extremely low affinity for σ2 receptor (K_i = 2.8 μM). KOR agonist 7 significantly reduces the secretion of pro-inflammatory cytokines such as IL-6, TNF-α, and IFN-γ, while increasing the production of the anti-inflammatory cytokine IL-10. KOR agonist 7 downregulates the expression of the pro-inflammatory M1 macrophage marker CD80 and upregulates the anti-inflammatory M2 macrophage marker CD163. KOR agonist 7 holds potential for applications in analgesia and immune modulation .

HY-B1076R

Medrysone (Standard) HMS (Standard); 6α-Methyl-11β-hydroxyprogesterone (Standard)	Reference Standards STAT VEGFR CCR	Inflammation/Immunology
Medrysone (Standard) is the analytical standard of Medrysone. This product is intended for research and analytical applications. Medrysone (HMS; 6α-Methyl-11β-hydroxyprogesterone) is a STAT6 modulator and M2 macrophage polarization inducer. Medrysone enhances IL-4-triggered STAT6 activation, upregulates the expression of M2 markers, and promotes the secretion of VEGF and CCL2. Medrysone also enhances the pro-migratory activity of M2-like macrophages toward endothelial cells. By regulating macrophage polarization and related repair pathways, Medrysone significantly promotes corneal wound repair in a rat mechanical injury model. Medrysone can be used for research related to corneal injury .

HY-143660

LG308	Microtubule/Tubulin Apoptosis	Cancer
LG308 is a novel synthetic compound with antimicrotubule activity. LG308 induces mitotic phase arrest and inhibits G2/M progression significantly which is associated with the upregulation of cyclin B1 and mitotic marker MPM-2 and the dephosphorylation of cdc2. LG308 also induces apoptosis and cell death. LG308 significantly suppresses tumor growth. LG308 with antimitotic activity has the potential for the research of prostate cancer .

HY-179049

EGFR/tubulin-IN-1	EGFR Microtubule/Tubulin Akt ERK Autophagy Atg8/LC3 p62 Ferroptosis Reactive Oxygen Species (ROS)	Cancer
EGFR/tubulin-IN-1 (Compound 26) is a dual-target inhibitor of EGFR and tubulin. EGFR/tubulin-IN-1 significantly reduces the levels of p-EGFR, p-AKT, and p-ERK in cells, disrupting the microtubule structure of the cells. EGFR/tubulin-IN-1 significantly inhibits the proliferation of H1975 cells and significantly blocks the cells in the G2/M phase. EGFR/tubulin-IN-1 induces the expression of autophagy markers LC3B-II and Beclin-1, while down-regulating the expression of p62. EGFR/tubulin-IN-1 induces ferroptosis, with increased ROS content and depletion of glutathione (GSH). EGFR/tubulin-IN-1 inhibits epithelial-mesenchymal transition (EMT) and tumor metastasis. EGFR/tubulin-IN-1 has a significant tumor-suppressing effect in the H1975 transplanted tumor nude mouse model. EGFR/tubulin-IN-1 can be used for the study of non-small cell lung cancer .

HY-181729

PROTAC BET Degrader-15	PROTACs Epigenetic Reader Domain Apoptosis c-Myc CDK PARP	Cancer
PROTAC BET Degrader-15 is a BET PROTAC degrader with DC₅₀ values of <0.10 nM, <0.01 nM, and <0.01 nM against BRD2, BRD3, and BRD4, respectively. PROTAC BET Degrader-15 induces significant G2/M phase cell cycle arrest and triggers apoptosis. PROTAC BET Degrader-15 causes marked downregulation of c-Myc, accompanied by upregulation of the cell cycle inhibitory protein p21, downregulation of CDK6, and an increase in the apoptosis marker cleaved PARP. PROTAC BET Degrader-15 is applicable to the research of hematologic malignancies and lung cancer .

HY-181076

FOXM1-IN-3	PI3K CDK Apoptosis	Cancer
FOXM1-IN-3 is a potent FOXM1 inhibitor. FOXM1-IN-3 downregulates FOXM1 expression at protein and mRNA levels, suppressing downstream effectors CCNB1 and CDC25. FOXM1-IN-3 induces G2/M cell cycle arrest and apoptosis in colorectal cancer cells. FOXM1-IN-3 inhibits colony formation and cell migration in colorectal cancer cells. FOXM1-IN-3 targets the cancer stem cell phenotype in colorectal cancer cells, reducing cancer stem cell marker expression. FOXM1-IN-3 reduces tumor growth in a zebrafish xenograft model. FOXM1-IN-3 can be used for the research of colorectal cancer .

Cat. No.	Product Name	Target	Research Area

HY-P11107

RP-832c	Apoptosis TNF Receptor	Inflammation/Immunology Cancer
RP-832c is a synthetic analogue of host defense peptides (HDP), targeting the mannose receptor CD206 on the surface of M2 polarized macrophages (K_d = 3.5 μM). RP-832c binding to CD206 induces a significant conformational change in the receptor, activating signaling pathways that lead to rapid apoptosis and repolarization of CD206-positive M2 macrophages to an M1 phenotype. RP-832c treatment significantly reduces CD206 gene expression in M2 macrophages while transiently increasing expression of TNF-α, a marker for M1 macrophages. RP-832c is used for the studies of T-cell lymphoma (CTCL) and idiopathic pulmonary fibrosis (IPF) .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N0430

Coptisine Coptisin	Alkaloids Structural Classification Classification of Application Fields Coptis chinensis Franch. Ranunculaceae Metabolic Disease Quinoline Alkaloids Plants Disease Research Fields Source Classification	Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR
Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .

HY-N0430A

Coptisine Sulfate 5 Publications Verification	Alkaloids Structural Classification Chelidonium majus Classification of Application Fields Metabolic Disease Quinoline Alkaloids Plants Disease Research Fields Papaveraceae Source Classification	Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR
Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a K_i of 5.8 μM and an IC₅₀ of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .

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