tgf-β 1 protein

BMT-124110 Formate is a selective AAK1 inhibitor (IC50: 0.9 nM) with anti-injury sensory activity.BMT-124110 Formate inhibits the BMP-2-inducible protein kinase BIKE with an IC50: 17 nM.BMT-124110 Formate inhibits the cell-cycle protein G-related BMT-124110 Formate inhibits the cell cycle protein G-associated kinase GAK with an IC50:99 nM.

SM1-71 is a potent multi-targeted acrylamide-modified TAK1 inhibitor that inhibits MKNK2, MAP2K1/2/3/4/6/7, GAK, AAK1, BMP2K, MAP3K7, MAPKAPK5, GSK3A/B, MAPK1/3, SRC, YES1, FGFR1, ZAK (MLTK), MAP3K1, LIMK1 and RSK2.SM1-71 can be used as a kinase probe with anticancer activity and inhibits the proliferation of various cancer cell lines.

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].

Sudubrilimab is an innovative bifunctional fusion protein designed to simultaneously target two key inhibitory pathways in the tumor microenvironment: the PD-1/PD-L1 immune checkpoint and the TGF-beta signaling axis. The compound consists of a humanized anti-PD-L1 monoclonal antibody fused to the extracellular domain of TGF-beta receptor II (TGFBR2-ECD). Serving as an essential tool for investigating the reversal of tumor immunosuppression and the enhancement of effector cell function, its design aims to overcome resistance to single-target therapies through synergistic action.

MY-673, a colchicine binding site inhibitor (CBSI), impedes tubulin polymerization and disrupts the ERK signaling pathway, consequently modulating SMAD4 protein expression in the TGF-β/SMAD pathway. This compound effectively reduces cell proliferation and migration while inducing apoptosis in both in vivo and in vitro settings [1].

Bintrafusp alfa (M7824) is a bifunctional fusion protein consisting of the extracellular structural domain of TGF-βRII (a TGF-β "trap") fused to a monoclonal antibody against human immunoglobulin G1 fused to programmed death ligand 1 (PD-L1), which is known for its anticancer activity, and can be used to study esophageal cancer. It has anticancer activity and can be used to study esophageal cancer.

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.

IMM-H007 is a novel lipid-lowering agent, increasing abca1 protein expression

Klotho-derived peptide 1 (KP1 human) hydrochloride inhibits the interaction between TGF-β and TGF-β receptor 2, suppressing the activation of TGF-β-induced Smad2/3 and mitogen-activated protein kinase (MAPK). Additionally, it exhibits antifibrotic and renal protective effects in mouse models.

Klotho-derived peptide 1 (KP1 human) can inhibit the interaction between TGF-β and its receptor TGF-β receptor 2, suppressing the activation of Smad2/3 and mitogen-activated protein kinase (MAPK) induced by TGF-β. It shows anti-fibrotic and renal protective effects in mouse models.