1158181-62-4
Chemical Structure
Relaxin H3 (human)
- CAS No.: 1158181-62-4
- Formula:C237H374N70O69S6
- Molecular Weight:5500.32
SMILES: O=C(N[C@@H](C)C(N[C@@H](C)C(N1[C@@H](CCC1)C(N[C@@H](CC2=CC=C(C=C2)O)C(NCC(N[C@@H](C(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC(C)C)C(N[C@@H](CSSC[C@@H](C(N[C@@H](CCCCN)C(N[C@@H](CC3=CNC4=CC=CC=C34)C(NC5)=O)=O)=O)NC([C@H](CSSC[C@@H](C(N[C@@H](CO)C(N[C@@H](CCCCN)C(N[C@@H](CO)C(N[C@@H](CCC(O)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CO)C(N[C@@H](CO)C(N[C@H]6CC(C)C)=O)=O)=O)=O)=O)=O)=O)=O)NC5=O)NC([C@H](CO)NC([C@H](CO)NC([C@H](CO)NC([C@H](CC(C)C)NC(CNC([C@H](C)NC([C@H](CC(C)C)NC([C@H](C(C)C)NC([C@H](CC(O)=O)N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)C(NCC(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC7=CC=CC=C7)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](C)C(N[C@@H](C(C)C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CC8=CC=CC=C8)C(N[C@@H]([C@H](O)C)C(N[C@@H](CSSC[C@@H](C(O)=O)NC6=O)C(NCC(NCC(N[C@@H](CO)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC9=CNC%10=CC=CC=C9%10)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)[C@H](CCCNC(N)=N)N
Biological Activity: Relaxin H3 (human) is a relaxin peptide with anti-inflammatory, anti-apoptotic, anti-pyroptotic, anti-migratory, protective and anti-fibrotic activities. Relaxin H3 (human) acts on RXFP1 to generate cAMP and reduce the levels of ATP and ROS. Relaxin H3 (human) inhibits renal inflammatory pyroptosis (pyroptosis), NLRP3 inflammasome activation, caspase-1 activation, IL-1β/IL-18 secretion, collagen synthesis, TGF-β1 signaling pathway, Smad2 phosphorylation, myofibroblast differentiation, TIMP expression, and HRMEC migration. Relaxin H3 (human) activates AMPK, upregulates MFN2 expression, improves mitochondrial quality control and membrane potential, inhibits apoptosis (apoptosis) and pyroptosis, restores retinal ultrastructure, and reverses excessive left ventricular collagen expression. Relaxin H3 (human) can be used in studies related to kidney stones, nephrocalcinosis, diabetic cardiomyopathy, fibrotic cardiomyopathy, and diabetic retinopathy[1][2][3][4][5].
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Relaxin H3 (human) | Relaxin H3 (human) is a relaxin peptide with anti-inflammatory, anti-apoptotic, anti-pyroptotic, anti-migratory, protective and anti-fibrotic activities. Relaxin H3 (human) acts on RXFP1 to generate cAMP and reduce the levels of ATP and ROS. Relaxin H3 (human) inhibits renal inflammatory pyroptosis (pyroptosis), NLRP3 inflammasome activation, caspase-1 activation, IL-1β/IL-18 secretion, collagen synthesis, TGF-β1 signaling pathway, Smad2 phosphorylation, myofibroblast differentiation, TIMP expression, and HRMEC migration. Relaxin H3 (human) activates AMPK, upregulates MFN2 expression, improves mitochondrial quality control and membrane potential, inhibits apoptosis (apoptosis) and pyroptosis, restores retinal ultrastructure, and reverses excessive left ventricular collagen expression. Relaxin H3 (human) can be used in studies related to kidney stones, nephrocalcinosis, diabetic cardiomyopathy, fibrotic cardiomyopathy, and diabetic retinopathy. | |||||||||||||||||||||
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- [1]. Liu J, et al. H3 relaxin protects against calcium oxalate crystal-induced renal inflammatory pyroptosis. Cell Prolif. 2020;53(10):e12902. [Content Brief]
- [2]. Zhang X, et al. H3 relaxin inhibits the collagen synthesis via ROS- and P2X7R-mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose. J Cell Mol Med. 2018 Mar;22(3):1816-1825. doi: 10.1111/jcmm.13464. Epub 2018 Jan 5. Erratum in: J Cell Mol Med. 2018 Jun;22(6):3264-3265. [Content Brief]
- [3]. Hossain MA, et al. H3 relaxin demonstrates antifibrotic properties via the RXFP1 receptor. Biochemistry. 2011;50(8):1368-1375. [Content Brief]
- [4]. Yang K, et al. H3 Relaxin Alleviates Migration, Apoptosis and Pyroptosis Through P2X7R-Mediated Nucleotide Binding Oligomerization Domain-Like Receptor Protein 3 Inflammasome Activation in Retinopathy Induced by Hyperglycemia. Front Pharmacol. 2020;11:603689. Published 2020 Dec 16. [Content Brief]
- [5]. Wang J, et al. H3 relaxin ameliorates mitochondrial quality control and apoptosis in cardiomyocytes of type 2 diabetic rats via activation of the AMPK pathway. Int Immunopharmacol. 2025;144:113664. [Content Brief]
Keywords
