Search Result

Results for "

myocardial fibrosis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adrenergic Receptor (2) Akt (5) Angiotensin-converting Enzyme (ACE) (1) Apoptosis (7) Autophagy (3) Bacterial (1) Caspase (1) Dopamine β-hydroxylase (2) Drug Metabolite (2) EGFR (1) Endogenous Metabolite (4) ERK (2) Ferroptosis (2) Glutathione Peroxidase (2) Guanylate Cyclase (1) Heme Oxygenase (HO) (2) Histone Demethylase (1) Indoleamine 2,3-Dioxygenase (IDO) (2) Keap1-Nrf2 (2) LXR (2) MMP (1) mTOR (3) NF-κB (2) NOD-like Receptor (NLR) (4) p38 MAPK (2) PERK (1) PI3K (3) Ras (1) Reactive Oxygen Species (ROS) (6) Reference Standards (2) Sirtuin (1) Src (2) STAT (3) TGF-beta/Smad (6) TGF-β Receptor (2) TRP Channel (1) Wnt (1)
By Research Areas:	Cancer (8) Cardiovascular Disease (18) Endocrinology (2) Infection (1) Inflammation/Immunology (10) Metabolic Disease (4) Neurological Disease (3)

By Targets:

Adrenergic Receptor (2)

Akt (5)

Angiotensin-converting Enzyme (ACE) (1)

Apoptosis (7)

Autophagy (3)

Bacterial (1)

Caspase (1)

Dopamine β-hydroxylase (2)

Drug Metabolite (2)

EGFR (1)

Endogenous Metabolite (4)

ERK (2)

Ferroptosis (2)

Glutathione Peroxidase (2)

Guanylate Cyclase (1)

Heme Oxygenase (HO) (2)

Histone Demethylase (1)

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

Keap1-Nrf2 (2)

LXR (2)

MMP (1)

mTOR (3)

NF-κB (2)

NOD-like Receptor (NLR) (4)

p38 MAPK (2)

PERK (1)

PI3K (3)

Ras (1)

Reactive Oxygen Species (ROS) (6)

Reference Standards (2)

Sirtuin (1)

Src (2)

STAT (3)

TGF-beta/Smad (6)

TGF-β Receptor (2)

TRP Channel (1)

Wnt (1)

By Research Areas:

Cancer (8)

Cardiovascular Disease (18)

Endocrinology (2)

Infection (1)

Inflammation/Immunology (10)

Metabolic Disease (4)

Neurological Disease (3)

Inhibitors & Agonists

Peptides

Natural
Products

Targets Recommended: CFTR

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-151483

TK-129	Wnt Histone Demethylase	Cardiovascular Disease
TK-129 is an orally active, low-toxicity, potent KDM5B inhibitor (with high affinity; IC₅₀=44 nM). TK-129 exerts cardioprotective effects by inhibiting KDM5B and blocking the KDM5B-associated Wnt pathway. TK-129 reduces ang II-induced activation of cardiac fibroblasts in vitro and reduces isoprenaline-induced myocardial remodelling and fibrosis in vivo. TK-129 can be used in studies of cardiovascular disease .

HY-158426

2-APQC 1 Publications Verification	Sirtuin	Cardiovascular Disease
2-APQC is an orally active and selective agonist of Sirtuin-3 (SIRT3) (K_d=2.756 μM), antagonizes Isoproterenol/ISO (HY-B0468)-induced cytotoxicity. 2-APQC activates the SIRT3-PYCR1 axis to enhance mitochondrial proline metabolism and inhibit the ROS-p38MAPK pathway by inhibiting signaling pathways such as mTOR-p70S6K, JNK, and TGF-β/Smad3. 2-APQC also activates the AMPK-Parkin axis to alleviate myocardial hypertrophy and fibrosis and protect cardiac function. 2-APQC can be used in the study of heart failure .

HY-N0202

Atractylenolide II 3 Publications Verification Asterolide	ERK Apoptosis p38 MAPK Akt Src STAT	Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
Atractylenolide II (Asterolide) is a sesquiterpenoid compound. Atractylenolide II can induce G1 phase cell cycle arrest and apoptosis in B16 melanoma cells. Atractylenolide II is an orally effective anticancer agent that can exert anti-melanoma effects by inhibiting the STAT3 signaling pathway. In addition, Atractylenolide II has been shown to ameliorate myocardial fibrosis, oxidative stress, and neuroprotective activity .

HY-122445

Resorcinolnaphthalein 2 Publications Verification	Angiotensin-converting Enzyme (ACE)	Cardiovascular Disease Inflammation/Immunology
Resorcinolnaphthalein is a specific angiotensin-converting enzyme 2 (ACE2) enhancer and activates ACE2 activity with an EC₅₀ value of 19.5 μM. Resorcinolnaphthalein can be used for the investigation of hypertension and renal fibrosis .

HY-128483

Fusaric acid	TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor	Cardiovascular Disease Endocrinology Cancer
Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β₁/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer .

HY-18282

AZ876	LXR	Cardiovascular Disease Metabolic Disease Cancer
AZ876 is a selective, orally active agonist of liver X receptor (LXRα/β) (K_i=0.007 μM [LXRα, human], 0.011 μM [LXRβ, human]. AZ876 induces the expression of target genes such as ABCA1 and ABCG1, promotes reverse cholesterol transport (RCT) and regulates lipid metabolism and anti-inflammatory effects. AZ876 increases cardiac polyunsaturated fatty acid levels, reduces myocardial fibrosis, and reduces lesion area and monocyte adhesion in atherosclerosis models. AZ876 can be used in cardiovascular disease research, such as preventing and treating β-adrenergic-induced cardiac diastolic dysfunction and inhibiting the progression of atherosclerosis .

HY-176267

AH001	Ras	Cardiovascular Disease
AH001 is a orally active RhoA inhibitor, which binds a cryptic pocket proximate to GDP within RhoA with a KD of 73.16 nM. AH001 interacts with GDP, stabilizing RhoA’s interaction with its endogenous inhibitor, RhoGDIα. AH001 reduces the downstream MRTFA nuclear translocation and downregulates fibrosis/hypertrophy proteins. AH001 mitigates myocardial remodeling in multiple HF animal models, and in the 3D myocardial tissue model. AH001 exerts its cardioprotective effects through the RhoA-RhoGDIα axis, effectively inhibiting downstream RhoA activation signaling.

HY-142698

SGC agonist 2	Guanylate Cyclase	Cardiovascular Disease
SGC agonist 2 is a potent agonist of soluble guanylate cyclase (SGC). Soluble guanylate cyclase is a key signal transduction enzyme in the NO-sGC-cGMP signaling pathway. SGC agonist 2 has the potential for the research of cardiovascular disease (heart failure, pulmonary hypertension, angina, myocardial infarction) and fibrotic diseases (renal fibrosis, systemic sclerosis) (extracted from patent WO2021219088A1, compound 031) .

HY-N0202R

Atractylenolide II (Standard) Asterolide (Standard)	ERK Reference Standards Apoptosis p38 MAPK Src Akt STAT	Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
Atractylenolide II (Standard) is the analytical standard of Atractylenolide II. This product is intended for research and analytical applications. Atractylenolide II (Asterolide) is a sesquiterpenoid compound. Atractylenolide II can induce G1 phase cell cycle arrest and apoptosis in B16 melanoma cells. Atractylenolide II is an orally effective anticancer agent that can exert anti-melanoma effects by inhibiting the STAT3 signaling pathway. In addition, Atractylenolide II has been shown to ameliorate myocardial fibrosis, oxidative stress, and neuroprotective activity .

HY-128483R

Fusaric acid (Standard)	TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor	Cardiovascular Disease Endocrinology Cancer
Fusaric acid (Standard) is the analytical standard of Fusaric acid (HY-128483). This product is intended for research and analytical applications. Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β₁/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer .

HY-108915

Trimethylamine N-oxide dihydrate Maximum Cited Publications 6 Publications Verification	NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Metabolic Disease Inflammation/Immunology
Trimethylamine N-oxide dihydrate is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide dihydrate induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide dihydrate also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .

HY-116084R

Trimethylamine N-oxide (Standard)	Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Inflammation/Immunology
Trimethylamine N-oxide (Standard) is the analytical standard of Trimethylamine N-oxide. This product is intended for research and analytical applications. Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .

HY-108915R

Trimethylamine N-oxide dihydrate (Standard)	NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Metabolic Disease Inflammation/Immunology
Trimethylamine N-oxide (dihydrate) (Standard) is the analytical standard of Trimethylamine N-oxide (dihydrate). This product is intended for research and analytical applications. Trimethylamine N-oxide dihydrate is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide dihydrate induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide dihydrate also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .

HY-116084

Trimethylamine N-oxide Maximum Cited Publications 6 Publications Verification	Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Inflammation/Immunology
Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .

HY-18282R

AZ876 (Standard)	LXR	Cardiovascular Disease Metabolic Disease Cancer
AZ876 (Standard) is the analytical standard of AZ876. This product is intended for research and analytical applications. AZ876 is a selective, orally active agonist of liver X receptor (LXRα/β) (Ki=0.007 μM [LXRα, human], 0.011 μM [LXRβ, human]. AZ876 induces the expression of target genes such as ABCA1 and ABCG1, promotes reverse cholesterol transport (RCT) and regulates lipid metabolism and anti-inflammatory effects. AZ876 increases cardiac polyunsaturated fatty acid levels, reduces myocardial fibrosis, and reduces lesion area and monocyte adhesion in atherosclerosis models. AZ876 can be used in cardiovascular disease research, such as preventing and treating β-adrenergic-induced cardiac diastolic dysfunction and inhibiting the progression of atherosclerosis .

HY-N0447

8-Gingerol 4 Publications Verification	TRP Channel Bacterial Apoptosis Autophagy STAT PERK EGFR PI3K Akt mTOR Caspase MMP	Infection Cardiovascular Disease Inflammation/Immunology Cancer
8-Gingerol can be found in the rhizome of ginger (Z. officinale) and has oral bioactivity. It activates TRPV1, with an EC₅₀ value of 5.0 µM. 8-Gingerol inhibits COX-2 and also suppresses the growth of H. pylori in vitro. Additionally, 8-Gingerol exhibits anticancer, antioxidant, and anti-inflammatory properties by inhibiting the epidermal growth factor receptor (EGFR) and modulating its downstream STAT3/ERK pathway to suppress the proliferation, migration, and invasion of colorectal cancer cells. 8-Gingerol also exerts immunosuppressive effects by inhibiting oxidative stress, inducing cell cycle arrest, promoting apoptosis, and regulating autophagy. Furthermore, 8-Gingerol has cardioprotective effects. 8-Gingerol is promising for research in the fields of cancer, infection, immunosuppression, and cardiovascular diseases.

HY-N0353R

Curdione (Standard) (+)-Curdione (Standard)	Reference Standards Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO)	Others
Curdione (Standard) is the analytical standard of Curdione. This product is intended for research and analytical applications. Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC₅₀ = 1.1 μM) and cyclooxygenase 2 expression .

HY-N0353

Curdione 1 Publications Verification (+)-Curdione	Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Autophagy Glutathione Peroxidase Keap1-Nrf2 Heme Oxygenase (HO) TGF-β Receptor Indoleamine 2,3-Dioxygenase (IDO)	Cardiovascular Disease Neurological Disease Cancer
Curdione ((+)-Curdione) is an orally active sesquiterpenoid. Curdione inhibits platelet aggregation. Curdione induces ferroptosis in colorectal cancer via m6A methylation mediated by METTL14 and YTHDF2. Curdione inhibits ferroptosis in Isoproterenol (HY-B0468)-induced myocardial infarction by regulating the Keap1/Trx1/GPX4 signaling pathway, suppressing oxidative stress (ROS) and apoptosis. Curdione ameliorates Doxorubicin (HY-15142)-induced cardiotoxicity by inhibiting oxidative stress (ROS) and activating the Nrf2/HO-1 pathway. Curdione ameliorates sepsis-induced lung injury by inhibiting platelet-mediated neutrophil extracellular trap formation. Curdione ameliorates Bleomycin (HY-17565A)-induced pulmonary fibrosis by inhibiting TGF-β-induced fibroblast-to-myofibroblast differentiation. Curdione exhibits neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats. Curdione exerts antiproliferative effects against human uterine leiomyosarcoma by targeting IDO1. Curdione protects vascular endothelial cells and atherosclerosis by regulating DNMT1-mediated ERBB4 promoter methylation. Curdione inhibits inducible prostaglandin E2 production (IC₅₀ = 1.1 μM) and cyclooxygenase 2 expression .

Cat. No.	Product Name	Target	Research Area

HY-P11206A

Murine cardiac troponin I peptide TFA Murine cardiac TnI peptide TFA	Peptides	Inflammation/Immunology
Murine cardiac troponin I peptide (Murine cardiac TnI peptide) TFA is a murine cardiac troponin I (cTnI) peptide. Murine cardiac troponin I peptide TFA can induce significant myocardial inflammation followed by fibrosis and heart failure with increased mortality in mice model. Murine cardiac troponin I peptide TFA can be used for heart failure research .

HY-P11206

Murine cardiac troponin I peptide Murine cardiac TnI peptide	Peptides	Cardiovascular Disease Inflammation/Immunology
Murine cardiac troponin I peptide (Murine cardiac TnI peptide) is a murine cardiac troponin I (cTnI) peptide. Murine cardiac troponin I peptide can induce significant myocardial inflammation followed by fibrosis and heart failure with increased mortality in mice model. Murine cardiac troponin I peptide can be used for heart failure research .

Cat. No.	Product Name	Category	Target	Chemical Structure