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Results for "

vascular smooth muscle growth

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

3

Peptides

2

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N2484
    Methylnissolin

    Astrapterocarpan

    		 PDGFR ERK Cardiovascular Disease
    Methylnissolin (Astrapterocarpan), isolated from Astragalus membranaceus, inhibits platelet-derived growth factor (PDGF)-BB-induced cell proliferation with an IC50 of 10 μM. Methylnissolin inhibits PDGF-BB-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERIC1/2) mitogen-activated protein (MAP) kinase. Methylnissolin inhibits PDGF-BB-induced vascular smooth muscle cell proliferation by inhibition of the ERK1/2 MAP kinase cascade .
    Methylnissolin
  • HY-12379
    NS-2028

    		Guanylate Cyclase Inflammation/Immunology
    NS-2028 is a highly selective soluble Guanylyl Cyclase (sGC) inhibitor with IC50 values of 30 nM and 200 nM for basal and NO-stimulated enzyme activity . NS-2028 inhibits soluble Guanylyl Cyclase activity in homogenates of mouse cerebellum and neuronal NO synthase with IC50 values of 17 nM and 20 nM . NS-2028 inhibits 3-morpholino-sydnonimine (SIN-1)-elicited formation of cyclic GMP in human cultured umbilical vein endothelial cells with an IC50 of 30 nM . NS-2028 is commonly used in the research of nitric oxide signaling pathways, it inhibits NO-dependent relaxant responses in non-vascular smooth muscle completely (1 μM) . NS-2028 reduces vascular endothelial growth factor-induced angiogenesis and permeability .
    NS-2028
  • HY-13948
    Angiotensin II human
    Maximum Cited Publications
    111 Publications Verification

    Angiotensin II; Ang II; DRVYIHPF

    		 Angiotensin Receptor Apoptosis Cardiovascular Disease Endocrinology Cancer
    Angiotensin II (Angiotensin II) is a vasoconstrictor and a major bioactive peptide of the renin/angiotensin system. Angiotensin II human plays a central role in regulating human blood pressure, which is mainly mediated by interactions between Angiotensin II and the G-protein-coupled receptors (GPCRs) Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). Angiotensin II human stimulates sympathetic nervous stimulation, increases aldosterone biosynthesis and renal actions. Angiotensin II human induces growth of vascular smooth muscle cells, increases collagen type I and III synthesis in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. Angiotensin II human also induces apoptosis. Angiotensin II induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway .
    Angiotensin II human
  • HY-13948A
    Angiotensin II human acetate
    Maximum Cited Publications
    111 Publications Verification

    Angiotensin II acetate; Ang II acetate; DRVYIHPF acetate

    		 Angiotensin Receptor Apoptosis Cardiovascular Disease Endocrinology Cancer
    Angiotensin II human (Angiotensin II) acetate is a vasoconstrictor and a major bioactive peptide of the renin/angiotensin system. Angiotensin II human acetate plays a central role in regulating human blood pressure, which is mainly mediated by interactions between Angiotensin II and the G-protein-coupled receptors (GPCRs) Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). Angiotensin II human acetate stimulates sympathetic nervous stimulation, increases aldosterone biosynthesis and renal actions. Angiotensin II human acetate induces growth of vascular smooth muscle cells, increases collagen type I and III synthesis in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. Angiotensin II human acetate also induces apoptosis. Angiotensin II human acetate induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway .
    Angiotensin II human acetate
  • HY-13948B
    Angiotensin II human TFA
    Maximum Cited Publications
    111 Publications Verification

    Angiotensin II TFA; Ang II TFA; DRVYIHPF TFA

    		 Angiotensin Receptor Apoptosis Cardiovascular Disease Endocrinology Cancer
    Angiotensin II human (Angiotensin II) TFA is a vasoconstrictor and a major bioactive peptide of the renin/angiotensin system. Angiotensin II human TFA plays a central role in regulating human blood pressure, which is mainly mediated by interactions between Angiotensin II and the G-protein-coupled receptors (GPCRs) Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). Angiotensin II human TFA stimulates sympathetic nervous stimulation, increases aldosterone biosynthesis and renal actions. Angiotensin II human TFA induces growth of vascular smooth muscle cells, increases collagen type I and III synthesis in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. Angiotensin II human TFA also induces apoptosis. Angiotensin II human TFA induces capillary formation from endothelial cells via the LOX-1 dependent redox-sensitive pathway .
    Angiotensin II human TFA
  • HY-134367
    Ap2A disodium

    		Others Cardiovascular Disease
    Ap2A (disodium) is a symmetrical dinucleoside polyphosphate. Ap2A (disodium) can promote the growth of vascular smooth muscle cells .
    Ap2A disodium
  • HY-134368
    Ap3A

    		Others Cardiovascular Disease
    Ap3A is a vasoactive molecule. Ap3A can promote the growth of vascular smooth muscle cells .
    Ap3A
  • HY-106890
    E4177

    57G709

    		 Angiotensin Receptor PDGFR Cardiovascular Disease
    E4177 (57G709) is an orally active angiotensin II receptor antagonist. E4177 can inhibit the growth of vascular smooth muscle cells (HASMC) and the increase of cell surface area. In addition, E4177 can also increase the expression of platelet-derived growth factor (PDGF) receptor. E4177 can be used in the study of vascular diseases .
    E4177
  • HY-106024A
    Alagebrium bromide

    ALT711 bromide

    		 Others Infection
    Alagebrium bromide is a cross-link breaker. This study investigated the role of advanced glycation end products (AGEs) in mediating protein kinase C (PKC) isoform expression in diabetic nephropathy. In vitro, vascular smooth muscle cells cultured in high glucose (25-mmol/l) showed increased translocation and expression of PKC-α compared with cells cultured in low glucose (5-mmol/l). Coculture with ALT-711 more effectively attenuated the increased expression and translocation of PKC-α compared with aminoguanidine, an inhibitor of AGE formation. Streptozotocin-induced diabetic rats were randomized to no treatment, ALT-711 treatment, or aminoguanidine treatment. Diabetes induced an increase in PKC-α as well as -βI, -βII, and -ε isoforms. ALT-711 and aminoguanidine treatment, both of which attenuated renal AGE accumulation, abolished these increases in PKC expression. However, only ALT-711 reduced the translocation of phosphorylated PKC-α from the cytoplasm to the membrane. ALT-711 treatment attenuated the expression of vascular endothelial growth factor (VEGF) and extracellular matrix proteins (fibronectin and laminin) and was associated with a reduction in albuminuria. Aminoguanidine had no effect on VEGF expression, although a reduction in fibronectin and laminin was observed. These findings suggest that AGEs are important stimulators of PKC activation, particularly PKC-α, in patients with diabetic nephropathy, which can be directly inhibited by ALT-711.
    Alagebrium bromide

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