uuo

R-268712 is a specific activin receptor-like kinase 5 (ALK5) inhibitor(IC50 of 2.5 nM). It is also an orally active transforming growth factor-β type I receptor inhibitor.

Trandolapril is an orally administered angiotensin converting enzyme (ACE) inhibitor that is hydrolysed to the active diacid trandolaprilat.

KS370G (Caffeic Acid Phenethyl Amide) inhibits UUO-induced renal fibrosis marker expression. KS370G is an orally active hypoglycemic and cardioprotective agent that reduces collagen deposition in obstructed kidneys and significantly decreases renal expression of inflammatory chemokines/adhesion molecules and monocyte markers and improves left ventricular hypertrophy and function in the heart of pressure-overloaded mice.KS370G can be used to study renal obstructive nephropathy.

BT424, a specific HCK inhibitor, modulates macrophage activation and autophagy in vitro, and mitigates inflammation and renal fibrosis in the UUO model [1].

Klotho-derived Peptide 1 (56-87) (human) TFA, a peptide derived from the human Klotho protein, disrupts TGF-β signaling through binding interactions with TGF-β receptor type 1 (TGFBR1) and TGF-β receptor type 2 (TGFBR2), with Kd values of 1.41 and 14.6 µM, respectively. Preincubation with Klotho-derived Peptide 1 (56-87) (human) TFA at 10 µg/mL inhibits TGF-β-induced increases in fibronectin and α-smooth muscle actin (α-SMA) expression in NRK-49F rat fibroblasts. In vivo investigations demonstrate that Klotho-derived Peptide 1 (56-87) (human) TFA, administered at 1 mg/kg per day, preferentially accumulates in damaged kidneys and significantly reduces serum creatinine and blood urea nitrogen levels while decreasing renal fibrosis in mouse models of unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury-induced renal fibrosis. Klotho-derived Peptide 1 (56-87) (human) TFA is therefore valuable for investigations involving renal fibrosis, TGF-β signaling modulation, and kidney injury-associated molecular pathways.