cardiac fibrosis

CCG-257081 (MRTF/SRF-IN-1) is an inhibitor of cardiac myosin-related transcription factor and serum response factor (MRTF/SRF) that acts by inhibiting the Rho/MRTF/SRF pathway.CCG-257081 has shown efficacy in preventing bleomycin-induced fibrosis in several mouse models. CCG-257081 can be used in cancer prevention and fibrosis research.

Canrenoate potassium (Soldactone) is a synthetic pregnadiene derivative with anti-aldosterone activity.

Sinapinic Acid (Synapoic acid) protects the rat liver from CCl4-induced inflammation, most likely by acting as a free radical scavenger and modulator of NF-κB p65 activation and proinflammatory cytokine expression. Sinapic acid with antioxidant role protects cardiac cells and its functions from I R induced oxidative stress. Sinapic acid is a potentially useful agent for the protection against liver fibrosis and cirrhosis. Sinapic acid prevents the alterations in the levels of lipids and lipoproteins by virtue of its anti-lipidaemic effect in isoproterenol induced myocardial infarcted rats. Sinapic acid ameliorates hyperglycemia through PLC-PKC signals to enhance the glucose utilization in diabetic rats.

Trimethylamine N-oxide dihydrate (TMANO Dihydrate), a product of the oxidation of trimethylamine, is considered as a protein stabilizer that may serve to counteract urea, the major osmolyte of sharks, skates and rays.

Ouabain octahydrate (Acocantherine) is a cardiac glycoside that inhibits Na(+) K(+) ATPase. Ouabain octahydrate regulates transcription of MDR (increase, Pgp) and MRP (increase MRP1 and decrease CFTR, cyctic fibrosis transport receptor or cAMP-activated Cl- channel) genes, also alters localization of MRP1.

IMM-H007 is a novel lipid-lowering agent, increasing abca1 protein expression

L002, a potent, cell-permeable, reversible, and specific acetyltransferase p300 (KAT3B) inhibitor with an IC50 of 1.98 μM, directly binds the acetyl-CoA pocket and competitively inhibits the FATp300 catalytic domain. By blocking histone acetylation, p53 acetylation, and STAT3 activation, L002 shows potential in the treatment of hypertension‐induced cardiac hypertrophy and fibrogenesis.

Hydrochlorothiazide (HCTZ) is a Thiazide Diuretic. The physiologic effect of hydrochlorothiazide is by means of Increased Diuresis.

EGFR-IN-542 is a novel EGFR inhibitor. EGFR-IN-542 significantly reduces myocardial inflammation, fibrosis, apoptosis and dysfunction. It shows promise for use in the treatment of obesity-induced cardiac complications.

TK-129 is an orally active, potent inhibitor of KDM5B with an IC50 of 44 nM and is low-toxicity. TK-129 exhibits cardioprotective effects by inhibiting KDM5B and blocking the KDM5B-associated Wnt pathway. TK-129 can be used in cardiovascular disease studies to reduce isoprenaline-induced myocardial remodelling and fibrosis in vivo, as well as to reduce ang II-induced activation of cardiac fibroblasts in vitro [1].

(R)-Fadrozole ((R)-CGS 16949A; FAD286) is a potent nonsteroidal inhibitor. (R)-Fadrozole also inhibits human placental aromatase (pIC 50 = 6.17) and aldosterone biosynthesis. (R)-Fadrozole reverses cardiac fibrosis in spontaneously hypertensive heart failure rats..

Trimethylamine N-oxide (TMAO) is a colorless amine oxide produced from choline, betaine, and carnitine via intestinal microbial metabolism that accumulates in tissues of marine animals and prevents the protein-damaging effects of urea.Trimethylamine N-oxide induces inflammation through activation of ROS NLRP3 inflammasomes, which can induce fibroblast differentiation and cardiac fibrosis.

Bixin is isolated from the seeds of Bixa orellana and possesses anti-tumor, anti-inflammatory, and antioxidant activities. Bixin treatment ameliorated cardiac dysfunction through inhibiting fibrosis, inflammation, and ROS generation.

ML334 (LH601A) is a transmembrane and potent NRF2 activator that inhibits Keap1-NRF2 protein interactions to ameliorate myocardial infarction-induced cardiac fibrosis by inhibiting cardiac fibroblast activation and proliferation.

Wnt signaling is required for direct multiple biological processes and also plays key roles in the pathogenesis of various diseases. Cyclic AMP response element-binding protein (CREB) is a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds as a homodimer to the cAMP-responsive element, an octameric palindrome. The protein is phosphorylated by several protein kinases, and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. Via generating a transcriptionally active complex with β-catenin, CREB acts as a mediator of Wnt signaling.ICG-001 is an inhibitor of β-catenin/CREB mediated transcription. The direct cellular target of ICG-001 is CREB. the inhibitory IC50of ICG-001 against β-catenin/CREB mediated transcription was 3 μM. ICG-001 treatment at the concentration of 25 μM for 24h significantly increased caspase activity in both colon cancer cell lines SW480 and HCT116 cell lines but not in normal colonic epithelial cells CCD-841Co. In a cell growth inhibition assay, the IC50s of ICG-001 against SW480 and HCT116 cells were 4.43 μM and 5.95 μM, respectively.In a SW620 nude mouse xenograft model, an water-soluble analog of ICG-001 given at the dose of 150 mg/kg i.v. once in every 2 days dramatically suppressed tumor growth. In a bleomycin-induced pulmonary fibrosis mice model, ICG-001 given at the dose of 5 mg/kg per day reversed pulmonary fibrosis. In a rat myocardial infarction model, ICG-001 was administrated subcutaneously at the dose of 50 mg/kg/day for 10 days which significantly improved cardiac contractile function after myocardial infarction in the rats.

(Rac)-Indoximod (1-Methyl-DL-tryptophan) is a potent inhibitor of indoleamine 2,3-dioxygenase (IDO). Combined treatment with IFN-γ and (Rac)-Indoximod significantly suppresses the activity of α-SMA-expressing human cardiac myofibroblasts (hCMs) and promotes apoptosis by up-regulating the genes IRF-1, Fas, and FasL, effectively improving cardiac fibrosis[1].