2. TGF-beta/Smad Apoptosis Immunology/Inflammation Cytoskeleton
  3. TGF-β Receptor Apoptosis Interleukin Related Integrin Cadherin
  4. THR-123

THR-123 is an orally active ALK3 peptide agonist. THR-123 has a relatively weak binding to ALK2, but does not bind to ALK6. THR-123 suppresses inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reverses established fibrosis in five mouse models of acute and chronic renal injury. THR-123 can be used for the study of kidney fibrosis.

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THR-123

THR-123 構造式

容量 在庫状況
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THR-123 関連抗体

Top Publications Citing Use of Products

TGF-β Receptor アイソフォーム固有の製品をすべて表示:

すべてのアイソフォームを表示
ALK1 ALK2 ALK3 ALK4 ALK5 ALK6 ALK7 TGFβR2 ACVR2A ACVR2B BMP

Interleukin Related アイソフォーム固有の製品をすべて表示:

すべてのアイソフォームを表示
IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

Integrin アイソフォーム固有の製品をすべて表示:

すべてのアイソフォームを表示
αvβ1 αvβ3 αvβ5 αvβ6 αvβ8 α5β1 α1β1 α2β1 α4β1 α9β1 αIIbβ3 α4β7 αLβ2

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製品説明

THR-123 is an orally active ALK3 peptide agonist. THR-123 has a relatively weak binding to ALK2, but does not bind to ALK6. THR-123 suppresses inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reverses established fibrosis in five mouse models of acute and chronic renal injury. THR-123 can be used for the study of kidney fibrosis[1].

IC50 & Target[1]

BMPR1A

 

IL-6

 

IL-8

 

体外実験

THR-123 (0-100 μM, 60 min) inhibits the expression of IL-6, IL-8 and ICAM-1 induced by TNF-α in a concentration-dependent manner in HK-2 cells[1].
THR-123 (250 μM) significantly inhibits TGF-β1, hypoxia, or cisplatin-induced cell apoptosis in HK-2 cells[1].
THR-123 (10 μM) restores the expression of E-cadherin inhibited by TGF-β1, reduces the expressions of CTGF and Snail1, and reverses the transformation of cell morphology into the mesenchymal form[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

THR-123 関連抗体
体内実験

THR-123 (5 mg/kg, p.o., once daily for 3 weeks) reverses renal fibrosis in mice with nephrotoxic serum-induced chronic kidney fibrosis (NTN)[1]. THR-123 (5 mg/kg, p.o., once daily for 7 days) significantly reduces renal tubular necrosis and tissue damage in ischemic re-perfusion injury (IRI) model in mice[1].
THR-123 (5-15 mg/kg, p.o. or i.p., once daily for 5-7 days) inhibits interstitial volume expansion and collagen deposition in unilateral ureteral obstruction (UUO) model in mice[1].
THR-123 (5 mg/kg, p.o., once daily from 8 weeks to 16 weeks of age) does not alter the glomerular abnormalities, and significantly inhibits the tubular atrophy and interstitial fibrosis seen in COL4A3KO mice[1].
THR-123 (5 mg/kg, p.o., once daily for 3 months) inhibits the progression of fibrosis associated with advanced diabetic nephropathy in mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Nephrotoxic serum nephritis, NTN model established in CD1 mice[1]
Dosage: 5 mg/kg
Administration: Oral administration (p.o.), once daily for 3 weeks
Result: Significantly reversed the already formed renal fibrosis, and improve glomerular sclerosis, renal tubular atrophy and interstitial fibrosis.
Significantly reduced renal function indicators.
Inhibited epithelial-mesenchymal transition (EMT) and reduce the number of E-cadherin and FSP1 double-positive renal tubular cells.
Reduced macrophage infiltration and activate the BMP-Smad signaling pathway (p-Smad1/5).
Animal Model: IRI model established in C57Bl/6 mice (8 weeks)[1]
Dosage: 5 mg/kg
Administration: Oral administration (p.o.), once daily for 7 days
Result: Significantly reduced the proportion of renal tubular necrosis and lowered the blood urea nitrogen level.
Reduced macrophage infiltration and alleviated cell apoptosis.
Animal Model: UUO model established in CD1 mice (8-12 week)[1]
Dosage: 5 and 15 mg/kg (p.o.) or 5 mg/kg (i.p.)
Administration: Oral administration (p.o.) or intraperitoneal injection (i.p.), once daily for 5-7 days
Result: Inhibited interstitial volume expansion and collagen deposition.
Reduced the expression of fibrosis markers (fibronectin and type I collagen).
Animal Model: Alport syndrome model established in eight weeks-old COL4A3KO mice on C57Bl/6 background[1]
Dosage: 5 mg/kg
Administration: Oral administration (p.o.), once daily from 8 weeks of age to 16 weeks of age
Result: Improved glomerular sclerosis, tubular damage and interstitial fibrosis.
Restored the expression of E-cadherin and reduce the fibroblast marker FSP1.
Animal Model: Streptozotocin (HY-13753) induced Diabetic nephropathy, DN model established in male CD1 mice (8 week)[1]
Dosage: 5 mg/kg
Administration: Oral administration (p.o.), once daily for 3 months
Result: Reduced mesangial matrix expansion, macrophage infiltration and cell apoptosis.
Delayed the deterioration of renal function in combination of Captopril (HY-B0368).
分子量

1926.13

分子式

C83H124N22O27S2
Sequence

Cys-Tyr-Phe-Asp-Asp-Ser-Ser-Asn-Val-Leu-Cys-Lys-Lys-Tyr-Arg-Ser (disulfide bridge: Cys1-Cys11)
Sequence Shortening

CYFDDSSNVLCKKYRS (disulfide bridge: Cys1-Cys11)
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

Please store the product under the recommended conditions in the Certificate of Analysis.
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参考文献
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THR-123 Related Classifications

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× = ×
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

THR-123THR123THR 123TGF-β ReceptorApoptosisInterleukin RelatedIntegrinCadherinTransforming growth factor beta receptorsILRenal FibrosisBMP SignalingEpithelial-to-Mesenchymal Transition (EMT)RegenerationInhibitorinhibitorinhibit

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THR-123
製品番号:
HY-P11354
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