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Results for "

cardiac fibrosis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Adenosine Receptor (1) AMPK (1) AP-1 (1) Apoptosis (4) Autophagy (1) Bacterial (1) Drug Metabolite (1) Endogenous Metabolite (4) ERK (2) Ferroptosis (1) Histone Acetyltransferase (1) Histone Demethylase (1) Indoleamine 2,3-Dioxygenase (IDO) (1) Isotope-Labeled Compounds (2) JAK (1) JNK (2) Mineralocorticoid Receptor (1) NF-κB (2) NOD-like Receptor (NLR) (4) Phosphatase (1) Phosphodiesterase (PDE) (2) Potassium Channel (6) Prostaglandin Receptor (1) Reactive Oxygen Species (6) Sirtuin (1) STAT (1) TGF-beta/Smad (11) TGF-β Receptor (1)
By Research Areas:	Cancer (8) Cardiovascular Disease (24) Infection (1) Inflammation/Immunology (12) Metabolic Disease (8)

By Targets:

Adenosine Receptor (1)

AMPK (1)

AP-1 (1)

Apoptosis (4)

Autophagy (1)

Bacterial (1)

Drug Metabolite (1)

Endogenous Metabolite (4)

ERK (2)

Ferroptosis (1)

Histone Acetyltransferase (1)

Histone Demethylase (1)

Indoleamine 2,3-Dioxygenase (IDO) (1)

Isotope-Labeled Compounds (2)

JAK (1)

JNK (2)

Mineralocorticoid Receptor (1)

NF-κB (2)

NOD-like Receptor (NLR) (4)

Phosphatase (1)

Phosphodiesterase (PDE) (2)

Potassium Channel (6)

Prostaglandin Receptor (1)

Reactive Oxygen Species (6)

Sirtuin (1)

STAT (1)

TGF-beta/Smad (11)

TGF-β Receptor (1)

By Research Areas:

Cancer (8)

Cardiovascular Disease (24)

Infection (1)

Inflammation/Immunology (12)

Metabolic Disease (8)

Inhibitors & Agonists

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: CFTR

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-B0252

Hydrochlorothiazide 3 Publications Verification HCTZ	TGF-beta/Smad Potassium Channel	Cardiovascular Disease Metabolic Disease Cancer
Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect .

HY-116084

Trimethylamine N-oxide 4 Publications Verification	Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species 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-108915

Trimethylamine N-oxide dihydrate 4 Publications Verification	NOD-like Receptor (NLR) Reactive Oxygen Species 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-151483

TK-129	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-N0617

Sanggenon C 2 Publications Verification	Phosphatase ERK NF-κB Apoptosis	Cardiovascular Disease Inflammation/Immunology Cancer
Sanggenon C, a flavonoid, exerts protective effects against cardiac hypertrophy and fibrosis via suppression of the calcineurin/NFAT2 pathway. Sanggenon C inhibits mitochondrial fission to induce apoptosis by blocking the ERK signaling pathway. Sanggenon C inhibits inducible nitric oxide synthase expression in RAW264.7 cells, and TNF-α-stimulated cell adhesion and VCAM-1 expression, by suppressing NF-κB activity. Sanggenon C possesses antioxidant, anti-inflammatory and antitumor activities .

HY-169026

DCN1-IN-2	TGF-beta/Smad	Cardiovascular Disease
DCN1-IN-2 is a DCN1 inhibitor with an IC₅₀ value of 2.96 nM. DCN1-IN-2 can alleviate Ang II/TGFβ-induced activation of cardiac fibroblasts. DCN1-IN-2 can reduce ISO-induced cardiac fibrosis and remodeling in mice by selectively inhibiting cullin 3 .

HY-123187

AS2553627	JAK	Cardiovascular Disease
AS2553627 is a type of JAK inhibitor, with IC₅₀ values of 0.46, 0.30, 0.14, and 2.0 nM for JAK1, JAK2, JAK3 and TYK2, respectively. AS2553627 can inhibit the proliferation of human and rat T cells stimulated by IL-2, with IC₅₀ values of 2.4 and 4.3 nM, respectively. AS2553627 can reduce cardiac allograft vasculopathy and fibrosis in a rat heart transplant model, effectively extending survival rates. AS2553627 can be used to prevent acute and chronic rejection in heart transplants .

HY-B0252S3

Hydrochlorothiazide-15N2,13C,d2 HCTZ-¹⁵N₂,¹³C,d₂	Potassium Channel TGF-beta/Smad Isotope-Labeled Compounds	Cardiovascular Disease Metabolic Disease Cancer
Hydrochlorothiazide- ¹⁵N₂, ¹³C,d₂ is ¹⁵N and deuterated labeled Hydrochlorothiazide (HY-B0252). Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect .

HY-162902

ALK5-IN-82	Others	Cardiovascular Disease
ALK5-IN-82 is a potent and selective inhibitor against activin receptor-like kinase 5 (ALK5) with an IC₅₀ value of 9.1 nM. ALK5-IN-82 inhibits the protein expression of α-smooth muscle actin (α-SMA), collagen I and tissue inhibitor of metalloproteinase 1 (TIMP-1)/matrix metalloproteinase 13 (MMP-13) in transforming growth factor-β-induced human umbilical vein endothelial cells. ALK5-IN-82 is promising for research of cardiac fibrosis .

HY-146205

ATX inhibitor 18	Phosphodiesterase (PDE)	Cardiovascular Disease
ATX inhibitor 18 is a potent ATX inhibitor with an IC₅₀ value of 24.2 nM. ATX inhibitor 18 shows antiproliferative activity and anti-fibrosis activity. ATX inhibitor 18 suppresses collagen deposition in TGF-β-mediated cardiac fibrosis .

HY-113986

Dexfadrostat (R)-Fadrozole; (R)-CGS 16949A free base; FAD286	Others	Cardiovascular Disease
Dexfadrostat ((R)-Fadrozole) is a potent nonsteroidal inhibitor . Dexfadrostat also inhibits human placental aromatase (pIC₅₀ = 6.17) and aldosterone biosynthesis. Dexfadrostat reverses cardiac fibrosis in spontaneously hypertensive heart failure rats. .

HY-N6884

Bixin 1 Publications Verification	Reactive Oxygen Species	Cardiovascular Disease Inflammation/Immunology Cancer
Bixin (BX), isolated from the seeds of Bixa orellana, is a carotenoid, possessing anti-inflammatory, anti-tumor and anti-oxidant activities. Bixin treatment ameliorated cardiac dysfunction through inhibiting fibrosis, inflammation and reactive oxygen species (ROS) generation .

HY-133897

(Rac)-Indoximod 1 Publications Verification 1-Methyl-DL-tryptophan; (Rac)-NLG-8189	Indoleamine 2,3-Dioxygenase (IDO) Apoptosis	Inflammation/Immunology Cancer
(Rac)-Indoximod (1-Methyl-DL-tryptophan) is an indoleamine 2,3-dioxygenase (IDO) inhibitor. Co-treatment with IFN-γ and (Rac)-Indoximod markedly reduces the activity of human cardiac myofibroblasts (hCMs) expressing α-SMA and induces apoptosis through up-regulating the IRF-1, Fas, and FasL genes .

HY-14858

Derenofylline SLV 320	Adenosine Receptor	Cardiovascular Disease
Derenofylline (SLV 320) is a potent, selective and orally active adenosine A₁ receptor antagonist, with K_i values of 1 nM, 200 nM and 398 nM for human A₁, A₃ and A_2A receptors respectively. Derenofylline suppresses cardiac fibrosis and attenuates albuminuria without affecting blood pressure in rats .

HY-100671

L002	Histone Acetyltransferase STAT	Inflammation/Immunology Cancer
L002 is a potent, cell permeable, reversible and specific acetyltransferase p300 (KAT3B) inhibitor with an?IC₅₀?of 1.98 μM . L002 binds the acetyl-CoA pocket and competitively inhibits the FATp300 catalytic domain, blocks histone acetylation and p53 acetylation, and inhibits STAT3 activation . L002 has the potential for hypertension‐induced cardiac hypertrophy and fibrogenesis treatment .

HY-B1582A

Canrenoate potassium Aldadiene potassium; SC-14266	Mineralocorticoid Receptor	Cardiovascular Disease
Canrenoate (Aldadiene) potassium, a proagent that releases canrenone, is a potent, competitive mineralocorticoid receptor (aldosterone receptor) antagonist. Potassium canrenoate, as a diuretic, is used for the research of hypertension .

HY-B0252S

Hydrochlorothiazid-d2 HCTZ-d₂	TGF-beta/Smad Potassium Channel	Cardiovascular Disease Metabolic Disease
Hydrochlorothiazid-d₂ is the deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

HY-N2329

Piperlongumine Maximum Cited Publications 7 Publications Verification Piplartine	ERK Reactive Oxygen Species Autophagy Apoptosis Bacterial Ferroptosis	Infection Cardiovascular Disease Cancer
Piperlongumine is a alkaloid , possesses ant-inflammatory, antibacterial, antiangiogenic, antioxidant, antitumor, and antidiabetic activities . Piperlongumine induces ROS, and induces apoptosis in cancer cell lines . Piperlongumine shows anti-cardiac fibrosis activity, suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway. Piperlongumin could be used in the study of migrasome .

HY-158426

2-APQC	Sirtuin	Cardiovascular Disease
2-APQC is a SIRT3 activator with the K_d value of 2.756 μM. 2-APQC improves heart failure in vitro and in vivo .

HY-B0252R

Hydrochlorothiazide (Standard) 3 Publications Verification HCTZ (Standard)	TGF-beta/Smad Potassium Channel	Cardiovascular Disease Metabolic Disease Cancer
Hydrochlorothiazide (Standard) is the analytical standard of Hydrochlorothiazide. This product is intended for research and analytical applications. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect .

HY-169052

Cyy-272	JNK Apoptosis	Cardiovascular Disease Inflammation/Immunology
Cyy-272 is an orally active JNK inhibitor with IC₅₀ values of 1.25 μM for JNK1, 1.07 μM for JNK2, and 1.24 μM for JNK3. Cyy-272 exerts anti-inflammatory effects by inhibiting JNK phosphorylation, thereby alleviating acute lung injury (ALI) induced by lipopolysaccharide (LPS, HY-D1056). Additionally, Cyy-272 significantly reduces inflammation in cardiomyocytes and cardiac tissue induced by high lipid concentrations, further mitigating cardiac hypertrophy, fibrosis, and apoptosis. Cyy-272 can be used in the study of obese cardiomyopathy .

HY-B0252S2

Hydrochlorothiazide-13C6 HCTZ-¹³C₆	TGF-beta/Smad Potassium Channel	Metabolic Disease
Hydrochlorothiazide- ¹³C₆ is the ¹³C labeled Hydrochlorothiazide[1]. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[2][3][4].

HY-B0252S1

Hydrochlorothiazid-13C,d2 HCTZ-¹³C,d₂	Isotope-Labeled Compounds TGF-beta/Smad Potassium Channel	Cardiovascular Disease Metabolic Disease
Hydrochlorothiazid- ¹³C,d₂ is the ¹³C- and deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

HY-116084S

Trimethylamine N-oxide-d9 1 Publications Verification	NOD-like Receptor (NLR) Reactive Oxygen Species TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Inflammation/Immunology
Trimethylamine N-oxide-d₉ is the deuterium labeled Trimethylamine N-oxide. 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[1][2][3].

HY-116084S1

Trimethylamine-N-oxide-13C3	NOD-like Receptor (NLR) Reactive Oxygen Species TGF-beta/Smad Endogenous Metabolite	Cardiovascular Disease Inflammation/Immunology
Trimethylamine-N-oxide- ¹³C₃ is the ¹³C-labeled Trimethylamine N-oxide. 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[1][2][3].

HY-119163

L-902688 2 Publications Verification	Prostaglandin Receptor	Cardiovascular Disease Inflammation/Immunology
L-902688 is a potent, selective and orally active EP4 receptor agonist with a K_i of 0.38 nM and an EC₅₀ of 0.6 nM. L-902688 shows >4,000-fold selective for EP4 over other EP and prostanoid receptors .

HY-133019

ATX inhibitor 5	Phosphodiesterase (PDE)	Inflammation/Immunology
ATX inhibitor 5 is a potent and orally active autotaxin (ATX) inhibitor, with an IC₅₀ of 15.3 nM. ATX inhibitor 5 shows anti-hepatofibrosis effects and reduces CCl4-induced hepatic fibrosis level prominently .

HY-141645

IMM-H007 WS070117	AMPK TGF-β Receptor NF-κB JNK AP-1	Cardiovascular Disease Metabolic Disease Inflammation/Immunology
IMM-H007 (WS070117) is an orally active and potent AMPK (AMP-activated protein kinase) activator and TGFβ1 (transforming growth factor β1) antagonist. IMM-H007 has protective effects in cardiovascular diseases via activation of AMPK. IMM-H007 negatively regulates endothelium inflammation through inactivating NF-κB and JNK/AP1 signaling. IMM-H007 inhibits ABCA1 degradation. IMM-H007 resolves hepatic steatosis in HFD-fed hamsters by the regulation of lipid metabolism. IMM-H007 can be used for the research of nonalcoholic fatty liver disease (NAFLD) and inflammatory atherosclerosis .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-116084

Trimethylamine N-oxide 4 Publications Verification	Cardiovascular Disease Structural Classification Natural Products Microorganisms Other disease Classification of Application Fields Source classification Disease markers Endogenous metabolite Inflammation/Immunology Disease Research Fields Cancer	Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species TGF-beta/Smad Endogenous Metabolite
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-108915

Trimethylamine N-oxide dihydrate 4 Publications Verification	Structural Classification Natural Products Classification of Application Fields Source classification Metabolic Disease Endogenous metabolite Disease Research Fields	NOD-like Receptor (NLR) Reactive Oxygen Species TGF-beta/Smad Endogenous Metabolite
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-N0617

Sanggenon C 2 Publications Verification	Cardiovascular Disease Structural Classification Classification of Application Fields Source classification Plants Moraceae Flavanonols Flavonoids Phenols Polyphenols Inflammation/Immunology Disease Research Fields Morus alba Linn.	Phosphatase ERK NF-κB Apoptosis
Sanggenon C, a flavonoid, exerts protective effects against cardiac hypertrophy and fibrosis via suppression of the calcineurin/NFAT2 pathway. Sanggenon C inhibits mitochondrial fission to induce apoptosis by blocking the ERK signaling pathway. Sanggenon C inhibits inducible nitric oxide synthase expression in RAW264.7 cells, and TNF-α-stimulated cell adhesion and VCAM-1 expression, by suppressing NF-κB activity. Sanggenon C possesses antioxidant, anti-inflammatory and antitumor activities .

HY-N6884

Bixin 1 Publications Verification	Bixaceae Bixa orellana Linn. Classification of Application Fields Ketones, Aldehydes, Acids Source classification Pigments Plants Inflammation/Immunology Disease Research Fields Cancer Food Research	Reactive Oxygen Species
Bixin (BX), isolated from the seeds of Bixa orellana, is a carotenoid, possessing anti-inflammatory, anti-tumor and anti-oxidant activities. Bixin treatment ameliorated cardiac dysfunction through inhibiting fibrosis, inflammation and reactive oxygen species (ROS) generation .

HY-N2329

Piperlongumine Maximum Cited Publications 7 Publications Verification Piplartine	Piper longum Linn. Infection Cardiovascular Disease Alkaloids Structural Classification Classification of Application Fields Source classification Pyridine Alkaloids Piperaceae Plants Disease Research Fields	ERK Reactive Oxygen Species Autophagy Apoptosis Bacterial Ferroptosis
Piperlongumine is a alkaloid , possesses ant-inflammatory, antibacterial, antiangiogenic, antioxidant, antitumor, and antidiabetic activities . Piperlongumine induces ROS, and induces apoptosis in cancer cell lines . Piperlongumine shows anti-cardiac fibrosis activity, suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway. Piperlongumin could be used in the study of migrasome .

Cat. No.	Product Name	Chemical Structure

HY-B0252S

Hydrochlorothiazid-d2
Hydrochlorothiazid-d₂ is the deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

Hydrochlorothiazid-d2

Hydrochlorothiazid-d₂ is the deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

HY-B0252S2

Hydrochlorothiazide-13C6
Hydrochlorothiazide- ¹³C₆ is the ¹³C labeled Hydrochlorothiazide[1]. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[2][3][4].

Hydrochlorothiazide-13C6

Hydrochlorothiazide- ¹³C₆ is the ¹³C labeled Hydrochlorothiazide[1]. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[2][3][4].

HY-116084S

Trimethylamine N-oxide-d9 1 Publications Verification
Trimethylamine N-oxide-d₉ is the deuterium labeled Trimethylamine N-oxide. 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[1][2][3].

Trimethylamine N-oxide-d9

1 Publications Verification

Trimethylamine N-oxide-d₉ is the deuterium labeled Trimethylamine N-oxide. 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[1][2][3].

HY-B0252S3

Hydrochlorothiazide-15N2,13C,d2
Hydrochlorothiazide- ¹⁵N₂, ¹³C,d₂ is ¹⁵N and deuterated labeled Hydrochlorothiazide (HY-B0252). Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect .

Hydrochlorothiazide-15N2,13C,d2

Hydrochlorothiazide- ¹⁵N₂, ¹³C,d₂ is ¹⁵N and deuterated labeled Hydrochlorothiazide (HY-B0252). Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect .

HY-B0252S1

Hydrochlorothiazid-13C,d2
Hydrochlorothiazid- ¹³C,d₂ is the ¹³C- and deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

Hydrochlorothiazid-13C,d2

Hydrochlorothiazid- ¹³C,d₂ is the ¹³C- and deuterium labeled Hydrochlorothiazide. Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].

HY-116084S1

Trimethylamine-N-oxide-13C3
Trimethylamine-N-oxide- ¹³C₃ is the ¹³C-labeled Trimethylamine N-oxide. 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[1][2][3].

Trimethylamine-N-oxide-13C3

Trimethylamine-N-oxide- ¹³C₃ is the ¹³C-labeled Trimethylamine N-oxide. 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[1][2][3].

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