176365-43-8
Chemical Structure
pUR4
- CAS No.: 176365-43-8
- Formula:C228H353N59O89S
- Molecular Weight:5376.65
SMILES: O=C(N[C@@H](CC(O)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](CO)C(N1[C@@H](CCC1)C(N[C@@H](CC(C)C)C(N[C@@H](C)C(NCC(N[C@@H](CCC(O)=O)C(N[C@@H](CO)C(NCC(N[C@@H](CCC(O)=O)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC2=CC=C(C=C2)O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](C(C)C)C(N[C@@H](CC3=CC=C(C=C3)O)C(NCC(N[C@@H](CC(N)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](CC(N)=O)C(N4[C@@H](CCC4)C(N[C@@H](C(C)C)C(N[C@@H](CC(O)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CC(O)=O)C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N5[C@@H](CCC5)C(N[C@@H](CC(N)=O)C(N[C@@H](CCC(O)=O)C(N[C@@H]([C@H](O)C)C(NCC(N[C@@H](CC6=CC=CC=C6)C(N[C@@H](CO)C(NCC(N[C@@H](CC(N)=O)C(N[C@@H](CCSC)C(N[C@@H](C(C)C)C(N[C@@H](CCC(O)=O)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H]([C@H](O)C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CCCCN)N
Biological Activity: pUR4 is a recombinant peptide that acts as a fibronectin (FN) inhibitor. pUR4 binds to the N-terminal type I modules of fibronectin, inhibiting the polymerization of soluble fibronectin and its deposition into the extracellular matrix (ECM). pUR4 reduces β1 integrin activation by depleting ECM fibronectin and disrupting FN-β1 integrin coupling. pUR4 attenuates TNF-α-induced endothelial hyperpermeability, maintains endothelial monolayer integrity, and reduces TNF-α-induced cell morphological changes. pUR4 decreases neutrophil adhesion to cardiac endothelial cells, T cell interstitial migration, immune cell infiltration, collagen deposition, and fibroblast activation. pUR4 can be used in research on pathological vascular leakage, heart failure, inflammation, chronic kidney disease, liver fibrosis, and intestinal fibrosis[1][2][3][4][5][6].
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pUR4 | pUR4 is a recombinant peptide that acts as a fibronectin (FN) inhibitor. pUR4 binds to the N-terminal type I modules of fibronectin, inhibiting the polymerization of soluble fibronectin and its deposition into the extracellular matrix (ECM). pUR4 reduces β1 integrin activation by depleting ECM fibronectin and disrupting FN-β1 integrin coupling. pUR4 attenuates TNF-α-induced endothelial hyperpermeability, maintains endothelial monolayer integrity, and reduces TNF-α-induced cell morphological changes. pUR4 decreases neutrophil adhesion to cardiac endothelial cells, T cell interstitial migration, immune cell infiltration, collagen deposition, and fibroblast activation. pUR4 can be used in research on pathological vascular leakage, heart failure, inflammation, chronic kidney disease, liver fibrosis, and intestinal fibrosis. | |||||||||||||||||||||
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References
- [1]. Lee TH, et al. Fibronectin inhibitor pUR4 attenuates tumor necrosis factor α-induced endothelial hyperpermeability by modulating β1 integrin activation. Journal of biomedical science. 2019 May 16;26(1):37.
- [2]. Valiente-Alandi I, et al. Inhibiting Fibronectin Attenuates Fibrosis and Improves Cardiac Function in a Model of Heart Failure. Circulation. 2018 Sep 18;138(12):1236-1252.
- [3]. Fernandes NRJ, et al. CD4 T Cell Interstitial Migration Controlled by Fibronectin in the Inflamed Skin. Frontiers in immunology. 2020;11:1501.
- [4]. Bowers SLK, et al. Inhibition of fibronectin polymerization alleviates kidney injury due to ischemia-reperfusion. Am J Physiol Renal Physiol. 2019 Jun 1;316(6):F1293-F1298.
- [5]. Altrock E, et al. Inhibition of fibronectin deposition improves experimental liver fibrosis. Journal of hepatology. 2015 Mar;62(3):625-33.
- [6]. Ma W, et al. Direct Extracellular Matrix Modulation Attenuates Intestinal Fibrosis via a Fibronectin-Targeted Approach. Advanced science (Weinheim, Baden-Wurttemberg, Germany). 2026 Apr;13(20):e19433.
