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Results for "

α-sma

" in TargetMol Product Catalog
  • Inhibitors & Agonists
    27
    TargetMol | Inhibitors_Agonists
  • Peptide Products
    2
    TargetMol | Peptide_Products
  • Natural Products
    2
    TargetMol | Natural_Products
Sinefungin
Antibiotic 32232RP, Adenosyl-Ornithine, A-9145
T1688658944-73-3In house
Sinefungin (Adenosyl-Ornithine) is an effective inhibitor of virion mRNA(guanine-7-)-methyltransferase, mRNA(nucleoside-2'-)-methyltransferase, and viral multiplication. Sinefungin is a SET7 9 inhibitor and ameliorates renal fibrosis by inhibiting H3K4 methylation.
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10-14 weeks
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Branaplam
NVS-SM1, LMI 070
T46411562338-42-4
Branaplam (LMI 070) is a highly potent, selective and orally active small molecule SMN2 splicing modulator.
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SRI-011381 hydrochloride
SRI-011381 hydrochloride [1629138-41-5(free base)]
T51292070014-88-7
SRI-011381 hydrochloride, a new-type agonist of the TGF-beta signaling pathway, is utilized in the treatment of Alzheimer's disease.
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TargetMol | Inhibitor Hot
Numidargistat dihydrochloride
INCB01158 dihydrochloride, INCB 01158 dihydrochloride, CB-1158 dihydrochloride ( free base), CB-1158 dihydrochloride, CB1158 dihydrochloride
T10692 In house
Numidargistat dihydrochloride (CB-1158 dihydrochloride) is an orally active and highly effective arginase (ARG1) inhibitor, an immuno-oncology agent that inhibits TGF-β2-induced subcapsular cataract by reducing the proliferation of lens epithelial cells (LEC) and decreasing the expression of fibronectin, α-SMA, collagen 1A1, and vimentin.
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TP-DEA2
T200593
TP-DEA2, a prodrug of triptolide, effectively inhibits bleomycin-induced pulmonary fibrosis and inflammatory responses. It significantly reduces the production of α-SMA.
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ALK5-IN-82
T2006043001361-04-9
ALK5-IN-82 is a potent and selective inhibitor of activin receptor-like kinase 5 (ALK5), demonstrating an IC50 value of 9.1 nM. This compound effectively suppresses the expression of α-smooth muscle actin (α-SMA), collagen I, and the proteinases tissue inhibitor of metalloproteinase 1 (TIMP-1) and matrix metalloproteinase 13 (MMP-13) in human umbilical vein endothelial cells induced by transforming growth factor-β. ALK5-IN-82 shows potential for use in research related to cardiac fibrosis.
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8-10 weeks
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JNK-1-IN-4
T2006673047795-60-5
JNK-1-IN-4 (Compound E1) is an inhibitor of JNK, targeting JNK-1, JNK-2, and JNK-3 with IC50 values of 2.7, 19.0, and 9.0 nM, respectively. This compound inhibits the phosphorylation of c-Jun and reduces the expression of TGF-β1-induced EMT markers (such as fibronectin and α-SMA). JNK-1-IN-4 exhibits favorable pharmacokinetic properties with a bioavailability of 69%. Additionally, it demonstrates antifibrotic effects in a Bleomycin-induced mouse model of idiopathic pulmonary fibrosis.
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8-10 weeks
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WQ-C-401
T2007662376694-72-1
WQ-C-401 is an orally active inhibitor of the platelet-derived growth factor receptor (PDGFR). It inhibits cell proliferation by blocking PDGFR auto-phosphorylation in a concentration-dependent manner, with EC50 values of 3.5 nM for PDGFRαY849 and 5.8 nM for PDGFRβY1021. Additionally, WQ-C-401 suppresses the proliferation and migration of PASMCs by inhibiting PDGF-BB-induced phosphorylation of ERK1 2, reduces collagen I synthesis, and increases α-SMA expression, thereby preventing pulmonary vascular remodeling. This compound shows promise for research in the field of pulmonary arterial hypertension.
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6-8 weeks
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GED-0507-34 Levo
Y4H78S56YZ, (S)-3-(4-Aminophenyl)-2-methoxypropanoicacid, (S)-3-(4-Aminophenyl)-2-methoxypropanoic acid
T202784921195-93-9
GED-0507-34 Levo ((S)-3-(4-Aminophenyl)-2-methoxypropanoic acid), an orally available PPARγ modulator for amelioration of inflammation-driven intestinal fibrosis, decreased the expression of the pro-fibrotic genes Acta2, COL1a1, and Fn1, reduced the protein levels of α-SMA and collagen I-II, the main markers of fibrosis, as well as the major components of the TGFβ Smad pathway, and decreased the expression of IL-13, CTGF, TGFB and ACTA1, and inhibited TGF-β-induced activation of fibroblasts and IECs cell lines.
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Anti-NASH agent 2
T2042533028778-28-8
Anti-NASH agent 2 (compound 21) is an inhibitor of neolipogenesis activity and α-SMA gene expression. It improves hepatic steatosis, edema, inflammatory infiltration, and liver fibrosis in NASH mouse models.
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10-14 weeks
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SIRT2-IN-17
T204843
SIRT2-IN-17 (compound Z18) is a potent inhibitor of SIRT2, effectively reducing the expression of α-SMA and p-Smad2 3.
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TRPV1-IN-3
T20520187657-67-8
TRPV1-IN-3 (compound 14) is a TRPV1 inhibitor utilized in idiopathic pulmonary fibrosis research. It demonstrates antifibrotic activity in vitro (IC50 = 0.51 μM) by inhibiting the TGF-β Smads and MAPK pathways, thereby affecting the expression of fibrosis markers collagen I and α-SMA. In vivo, TRPV1-IN-3 significantly reduces collagen deposition in lung tissue, improves alveolar structure, and increases survival rates in mice with Bleomycin-induced pulmonary fibrosis.
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10-14 weeks
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FGFRs-IN-1
T205323
FGFRs-IN-1 (Compound A16) is an orally active inhibitor targeting FGFR1 2 3 4, with IC50 values of 2.3, 7, 11, and 163 nM respectively. It also inhibits VEGFR1 2 3, Abl, and Flt3, with IC50 values of 61, 176, 112, 26, and 353 nM. The compound shows weak inhibition of CYP enzymes. FGFRs-IN-1 reduces the expression of α-SMA and collagen I, and it inhibits epithelial-mesenchymal transition (EMT) in A549 cells stimulated by TGF-β1. Additionally, FGFRs-IN-1 demonstrates anti-inflammatory activity in mouse models of lung fibrosis induced by Bleomycin and liver fibrosis induced by CCl4.
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C18 dihydro Ceramide (d18:0/18:0)
C18 dihydro Ceramide (d18:0 18:0),Cer(d18:0 18:0)
T358072304-80-5
C18 dihydro Ceramide is a bioactive sphingolipid and precursor in the de novo synthesis of C18 ceramide that lacks the 4,5-trans double bond. [1] Increased C18 dihydroceramide lipid levels lead to increased triacylglycerol storage and autophagosome accumulation as well as upregulation of the fibrosis markers α-SMA and FGF2 in Chang and LX-2 liver cells. C18 dihydro Ceramide is elevated in the plasma of pre-diabetics up to 9 years prior to the onset of type 2 diabetes. [2] It is also elevated in the skin of patients with lesional atopic dermatitis.[3]
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7-10 days
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SRI-011381
T42831629138-41-5
SRI-011381, a new-type agonist of the TGF-beta signaling pathway, is utilized in the treatment of Alzheimer's disease.
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TargetMol | Inhibitor Sale
Loureirin A
T5S0896119425-89-7
Loureirin A has an inhibitory effect on platelet activation, perhaps through an impairment of PI3K Akt signaling.Loureirin A negatively affects agonist-induced platelet aggregation such as collagen, collagen-related peptide (CRP), ADP and thrombin. Lourei
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(Rac)-Indoximod
T6026626988-72-7
(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].
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6-8 weeks
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TGFβ1-IN-1
T613892348795-14-0
TGFβ1-IN-1 is an orally active TGF-β1 inhibitor that inhibits the production of TGF-β1-induced fibrotic markers (α-SMA and fibronectin) and can be used for the study of cancer and autoimmune diseases.
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10-14 weeks
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TGFβ-IN-2
T615862387678-02-4
TGFβ-IN-2 (Compound 9d) effectively inhibits TGF-β-induced accumulation of total collagen in NRK-49F cells, with an IC50 value of 4.31 μM. It also suppresses the TGF-β-induced in vitro expression of COL1A1, α-SMA, and p-Smad3. Additionally, TGFβ-IN-2 shows promise as a potential anti-fibrosis compound for in vivo applications through oral administration [1].
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6-8 weeks
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NTU281
T63248815619-12-6
NTU281 is a potent inhibitor of transglutaminase-2 that reduces the elevation of serum creatinine and proteinuria in diabetic rats and decreases glomerular type I collagen accumulation, Hic-5 and α-SMA expression, as well as apoptosis, and can be used in studies of diabetes-induced glomerulosclerosis.
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10-14 weeks
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atx inhibitor 11
T641412485779-27-7
ATX inhibitor 11 is a potent inhibitor of ATX (autotaxin) (IC50: 2.7 nM). ATX inhibitor 11 alleviates the severity of fibrotic tissue and effectively reduces the deposition of α-SMA, a biomarker of fibrosis, in a mouse model of fibrosis. ATX inhibitor 11 can be used to study lung fibrosis.
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6-8 weeks
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FXR agonist 3
T74996
FXR agonist 3 is an anti-NASH compound with antifibrotic and anti-fibrotic activity, inhibiting the expression of COL1A1, TGF-β1, α-SMA, and TIMP1, with an IC50 value of 8.19 μmol L for COL1A1. FXR agonist 3 ameliorates CDAHFD and BDL-induced liver injury in vivo by activating FXR.
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7-10 days
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Tat-Gap 19 TFA
T83682
Tat-Gap 19, a peptide inhibitor of connexin43 (Cx43) hemichannels, is derived from the HIV-1 Tat protein transduction domain fused with a nine-amino acid sequence from Cx43 residues 128-136. This compound, at a concentration of 10 µM, effectively suppresses glutamate-induced ATP release in primary rat hepatocytes, indicating inhibition of Cx43 hemichannel activity. Furthermore, Tat-Gap 19 demonstrates therapeutic potential by significantly reducing infarct volume in a mouse cerebral ischemia-reperfusion injury model following middle cerebral artery occlusion (MCAO) at a dosage of 25 mg/kg. Moreover, its intraperitoneal administration at 1 mg/kg per day ameliorates fibrosis and decreases the area of hepatic stellate cells, the precursors to myofibroblasts, expressing α-smooth muscle actin (α-SMA), in a model of thioacetamide-induced liver damage. Additionally, it enhances superoxide dismutase (SOD) activity in hepatic cells from the treated mice, indicating its antioxidative benefits.
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Klotho-derived Peptide 1 (56-87) (human) TFA
KP1 (56-87)
T83770
Klotho-derived peptide 1 (KP1) (56-87), a peptide originating from the human Klotho protein, disrupts TGF-β signaling by binding to TGF-β receptor types 1 and 2 (TGFBR1 and TGFBR2; Kds = 1.41 and 14.6 µM, respectively). Preincubation with KP1 at a concentration of 10 µg/ml hinders the TGF-β-induced escalation of fibronectin and α-smooth muscle actin (α-SMA) levels in NRK-49F rat fibroblasts. Furthermore, in vivo studies reveal that KP1, administered at 1 mg/kg per day, preferentially accumulates in damaged kidneys, leading to significant reductions in serum creatinine and blood urea nitrogen levels, indicators of improved kidney function. Additionally, it decreases kidney fibrosis in mouse models of unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury-induced renal fibrosis.
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