PI-201

PI-201

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Category Bioactive by-products
Catalog number BBF-03344
CAS 143605-56-5
Molecular Weight 280.4
Molecular Formula C17H28O3

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Description

PI-201 is a platelet aggregation inhibitor produced by Streptomyces sp. A7498. It inhibited ADP-induced aggregation of rabbit platelets with IC50 of 7.1 x 10(-4) M.

Specification

Synonyms PI 201; PI201
IUPAC Name methyl (1S,2R,4aS,8aR)-2-[(2R)-2-hydroxybutyl]-3-methyl-1,2,4a,5,6,7,8,8a-octahydronaphthalene-1-carboxylate
Canonical SMILES CCC(CC1C(C2CCCCC2C=C1C)C(=O)OC)O
InChI InChI=1S/C17H28O3/c1-4-13(18)10-15-11(2)9-12-7-5-6-8-14(12)16(15)17(19)20-3/h9,12-16,18H,4-8,10H2,1-3H3/t12-,13-,14-,15+,16+/m1/s1
InChI Key UMSPFLJZBBTPKA-SUJAAXHWSA-N

Properties

Appearance Colorless Crystal

Reference Reading

1. Liver cold preservation induce lung surfactant changes and acute lung injury in rat liver transplantation
An Jiang, Chang Liu, Feng Liu, Yu-Long Song, Quan-Yuan Li, Liang Yu, Yi Lv World J Gastroenterol. 2012 Jan 28;18(4):323-30. doi: 10.3748/wjg.v18.i4.323.
Aim: To investigate the relationship between donor liver cold preservation, lung surfactant (LS) changes and acute lung injury (ALI) after liver transplantation. Methods: Liver transplantation models were established using male Wistar rats. Donor livers were preserved in University of Wisconsin solution at 4 °C for different lengths of time. The effect of ammonium pyrrolidinedithiocarbamate (PDTC) on ALI was also detected. All samples were harvested after 3 h reperfusion. The severity of ALI was evaluated by lung weight/body weight ratio, lung histopathological score, serum nitric oxide (NO) and endothelin (ET)-1 levels, lung tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels. Lung surfactants (LSs) were determined by micellar electrokinetic capillary chromatography. Results: With extended donor liver cold preservation time (CPT), lung histopathological scores, serum ET-1 levels, lung weight/body weight ratio and the level of TNF-α and IL-1β in lung were increased significantly in the 180-min group compared with the sham group (3.16 ± 0.28 vs 1.12 ± 0.21, P < 0.001; 343.59 ± 53.97 vs 141.53 ± 48.48, P < 0.001; 0.00687 ± 0.00037 vs 0.00557 ± 0.00056, P < 0.001; 17.5 ± 3.0 vs 1.3 ± 0.3, P < 0.001; 10.8 ± 2.3 vs 1.8 ± 0.4, P < 0.001), but serum NO levels decreased remarkably (74.67 ± 10.01 vs 24.97 ± 3.18, P < 0.001). The expression of lung phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI) and phosphatidylserine (PS) increased when CPT was < 120 min, and decreased when CPT was > 180 min (PC: 1318.89 ± 54.79 vs 1011.18 ± 59.99, P < 0.001; PE: 1504.45 ± 119.96 vs 1340.80 ± 76.39, P = 0.0019; PI: 201.23 ± 34.82 vs 185.88 ± 17.04, P = 0.2265; PS: 300.43 ± 32.95 vs 286.55 ± 55.55, P = 0.5054). All these ALI-associated indexes could be partially reversed by PDTC treatment. Conclusion: Prolonged CPT could induce or inhibit the expression of LSs at the compensation or decompensation stage, and some antioxidants (e.g., PDTC) may reverse the pathological process partially.
2. PI-200 and PI-201, new platelet aggregation inhibitors produced by Streptomyces sp. A7498. Taxonomy, fermentation, isolation, physico-chemical properties, structure determination and biological properties
Y Kishimura, A Kawashima, T Kagamizono, M Yamagishi, K Matsumoto, Y Kawashima, K Hanada J Antibiot (Tokyo). 1992 Jun;45(6):892-8. doi: 10.7164/antibiotics.45.892.
Two new platelet aggregation inhibitors, PI-200 and PI-201 were isolated from the fermentation broth of Streptomyces sp. A7498. PI-200 and PI-201 inhibited ADP-induced aggregation of rabbit platelets with an IC50 of 3.8 x 10(-4) M and 7.1 x 10(-4) M, respectively.

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Tip: Chemical formula is case sensitive. C22H30N4O c22h30n40
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