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Request The Product List ofFibrosis Fibrosis

   Fibrosis is defined by the deposition of pathological fibrillar collagen, inflammatory cells, loss of capillaries, and dedifferentiation of epithelial cells.


   Fibrosis occurs as a part of normal wound healing. However, excessive or dysregulated fibrosis can lead to severe organ dysfunction and is a feature of a variety of diseases. Due to its insidious onset, fibrosis tends to go undetected in its early stages. This is in part why these diseases remain so poorly understood. Animal models have provided a means to examine these early stages and to isolate and understand the effect of perturbations in signaling pathways, chemokines, and cytokines. Here, we summarize recent progress in the understanding of the molecular pathogenesis of fibrosis, both its initiation and its maintenance phases, from animal models of fibrosis in the skin and liver. Due to these organs’ properties, modeling fibrosis in them poses unique challenges. Elegant solutions have therefore been developed for modeling fibrosis in each, and now, great potential for animal models to contribute to our understanding appears scientifically imminent.

Cat. No. Product Name CAS No. Information
GY03957

Lumacaftor

936727-05-8

VX-809 (Lumacaftor, VRT 826809) is a potent CFTR corrector that increases F508del-CFTR-mediated chloride transport amd improves F508del-CFTR maturation in FRT cells with EC50 of 0.1 and 0.5 uM, respectively; improves F508del-CFTR processing in the endoplasmic reticulum and enhances chloride secretion to approximately 14% of non-CF human bronchial epithelial cells (EC50=81 nM); exhibits biochemical and functional characteristics similar to normal CFTR, including biochemical susceptibility to proteolysis, residence time in the plasma membrane, and single-channel open probability after F508del-CFTR corrected by VX-809.

GY06694

Cavosonstat

1371587-51-7

Cavosonstat (N91115, N-91115) is a potent, orally bioavailable inhibitor of S-nitrosoglutathione reductase (GSNOR) and CFTR modulator; promotes CFTR maturation and plasma membrane stability, with a mechanism of action complementary to CFTR correctors and potentiators; significantly increases cell surface expression of F508del-CFTR in vitro combined with CFTR correctors.

GY06683

PBI-4050

1002101-19-0

PBI-4050 (Setogepram, PBI4050) is a synthetic analog of a medium-chain fatty acid that displays agonist and antagonist ligand affinity toward GPR40 and GPR84, respectively; PBI-4050 significantly attenuated fibrosis in many injury contexts, as evidenced by the antifibrotic activity observed in kidney, liver, heart, lung, pancreas, and skin fibrosis models; PBI-4050 is a first-in-class compound that may be effective for managing inflammatory and fibrosis-related diseases.

GY06651

PBI-4050 sodium

1254472-97-3

PBI-4050 (Setogepram, PBI4050) is a synthetic analog of a medium-chain fatty acid that displays agonist and antagonist ligand affinity toward GPR40 and GPR84, respectively; PBI-4050 significantly attenuated fibrosis in many injury contexts, as evidenced by the antifibrotic activity observed in kidney, liver, heart, lung, pancreas, and skin fibrosis models; PBI-4050 is a first-in-class compound that may be effective for managing inflammatory and fibrosis-related diseases.

GY06621

TD-139

1450824-22-2

TD-139 (TD139) is a highly potent, selecitve inhibitor of Galectin-3 (Gal-3) carbohydrate binding domain with Ki of 14 nM; reduces TGF-β1-induced β-catenin translocation to the nucleus, blocks β-catenin phosphorylation in vitro and in vivo; attenuates the late-stage progression of lung fibrosis in murine models; attenuates liver injury and milder infiltration of IFNγ- and IL-17- and -4-producing CD4(+) T cells, increases IL-10-producing CD4(+) T cells and F4/80(+) CD206(+) alternatively activated macrophages and prevents the apoptosis of liver-infiltrating MNCs in WT C57BL/6 mice.

GY02316

BMS-986020

1257213-50-5

BMS-986020 (BMS986020, AM-152) is a potent, selective, orally available LPA1 receptor antagonist for treating idiopathic pulmonary fibrosis.

GY02051

INT-767

1000403-03-1

INT-767 is a potent, selective, dual farnesoid X receptor (FXR) and TGR5 agonist with EC50 of 30 and 630 nM, respectively; fails to activate 15 other nuclear receptors involved in metabolic pathways, and does not inhibit cytochrome P450 enzymes; induces FXR-dependent lipid uptake by adipocytes and promotes TGR5-dependent glucagon-like peptide-1 (GLP-1) secretion by enteroendocrine cells; markedly decreases cholesterol and triglyceride levels in diabetic db/db mice.

GY05214

Olacaftor

1897384-89-2

Olacaftor (VX-440, VX440) is a next-generation CFTR corrector, shows the potential to enhance the amount of CFTR protein at the cell’s surface and for treatment of cystic fibrosis.

GY04100

Ivacaftor

873054-44-5

Ivacaftor (VX-770, VX770) is a potent, orally bioavailable CFTR potentiator, increases G551D- and F508del CFTR-mediated Cl- secretion with EC50 of 100 nM; increases CFTR channel open probability (Po) in both the F508del processing mutation and the G551D gating mutation in recombinant cells, increases the Po of G551D CFTR by 6-fold, the Po of F508del- and wild-type CFTR by 5-fold and 2-fold, respectively; also potentiates CFTR-mediated Cl− secretion in primary cultures of G551D/F508del HBE and F508del HBE; demonstrates potential for treatment of cystic fibrosis with certain mutations in CFTR gene (primarily the G551D mutation).

GY05362

Ivacaftor hydrate

1134822-07-3

Ivacaftor (VX-770, VX770) is a potent, orally bioavailable CFTR potentiator, increases G551D- and F508del CFTR-mediated Cl- secretion with EC50 of 100 nM; increases CFTR channel open probability (Po) in both the F508del processing mutation and the G551D gating mutation in recombinant cells, increases the Po of G551D CFTR by 6-fold, the Po of F508del- and wild-type CFTR by 5-fold and 2-fold, respectively; also potentiates CFTR-mediated Cl− secretion in primary cultures of G551D/F508del HBE and F508del HBE; demonstrates potential for treatment of cystic fibrosis with certain mutations in CFTR gene (primarily the G551D mutation).

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