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Detail of "745-65-3"

  • MSDS Download
  • CAS Number:
  • 745-65-3
  • Name:
  • Prostaglandin E1

  • Molecular Structure:
  • Formula:
  • C20H34O5
  • Molecular Weight:
  • 354.49
  • Deleted CAS:
  • 22299-37-2|50-83-9|50865-30-0
  • Synonyms:
  • Cyclopentaneheptanoicacid, 3-hydroxy-2-(3-hydroxy-1-octenyl)-5-oxo-, (-)- (8CI);Cyclopentaneheptanoicacid, 3a-hydroxy-2-(3-hydroxy-1-octenyl)-5-oxo-(7CI);(-)-Prostaglandin E1;11a,15(S)-Dihydroxy-9-oxo-13-trans-prostenoic acid;11a,15a-Dihydroxy-9-oxo-13-trans-prostenoic acid;Alprox TD;Caveject;Caverject;Eglandin;Liple;Lipoprost;Liprostin;Minprog;NSC 165559;ONO 1608;Palux;Prostandin 500;Prostin VR Pediatric;Prostivas;SEPA-PGE1;SEPA-alprostadil;Topiglan;Vasaprostan;l-PGE1;l-Prostaglandin E1;
  • EINECS:
  • 212-017-2
  • Density:
  • 1.131 g/cm3
  • Melting Point:
  • 115-116 °C
  • Boiling Point:
  • 529.3 °C at 760 mmHg
  • Flash Point:
  • 288 °C
  • Solubility:
  • insoluble in water
  • Appearance:
  • Crystalline solid
  • Hazard Symbols:
  • HarmfulXn, IrritantXi
  • Risk Codes:
  • 22-36/37/38
  • Safety:
  • 36-26 Details
  • Transport Information:
  • UN 2811 6.1/PG 3

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CAS No.745-65-3 Prostaglandin E1Competitive Product

Assay:99%  Appearance:white powder  Package:1g/bag ,5g/b...

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CAS No.745-65-3 Prostaglandin E1Competitive Product

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CAS No.745-65-3 Prostaglandin E1

  Appearance:Crystal

Prostaglandin E1 (PGE1) Characteristics melting point 115-116℃. Action and use PGE1 is a natural prostaglandin with a strong effect on blood vessel diastolization, smooth muscle loosening and platelet agglutination inhibition. Its effect on bronchodilatation is 10 to 100 time

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CAS No.745-65-3 Prostaglandin E1

Category : Intermediates/Pharmaceutical intermediates CAS NO : 745-65-3 EC NO : 212-017-2 MF : C20H33O5 MW : 353.4736 Synonyms : ALPROSTADIL;Prostaglandin E1 or AIPROSTADIL;Alprostadil (prostandin E1);11,15-dihydroxy-9-oxoprost-13-en-1-oic acid;(11alpha,15S)-11,15-dihydr

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CAS 745-65-3 Alprostadil (prostandin E1)

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Product No: BBTA-003 Product name: Prostaglandin E1 Synonyms: 3-Hydroxy-2-(3-hydroxy-1-octenyl)-5-oxo-cyclopentaneheptanoic acid; 11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid; Molecular formula: C20H34O5 Molecular weight : 354.48 EINECS 212-017-2 Melting point: 115-116 oC

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Assay:99%  Appearance:white powder

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CAS No.745-65-3 Prostaglandin E1

Name:Alprostadil, (PGE1), Prostaglandin E1 CAS No:745-65-3 M.W.:354.9 M.W.:C20H34O5 Standard: USP30

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CAS No.745-65-3 Prostaglandin E1

Alprostadil Cas No.:745-65-3 Content:99% Standard:USP30 Molecular Formula:C20H34O5?Molecular Weight:354.49? Appearance: white to off-white crystalline powder.

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C20 H34 O5

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Reference

Macrophage aggregation induced by the human lymphokine, macrophage aggregating factor
Macrophage aggregation induced by the human lymphokine, macrophage aggregating factor.Some chemicals with cas registry numbers like 9029-60-1 and 745-65-3 are also used. Role of the eicosanoid system. Rouveix, B.; Larno, S.; Lechat, P. (Dep. Pharmacol. Clin., Hop. Claude-Bernard, Paris F 75944, Fr.). J. Pharmacol., 14(4), 473-84 (French) 1983. CODEN: JNPHAG. ISSN: 0021-793X. DOCUMENT TYPE: Journal CA Section: 15 (Immunochemistry) Section cross-reference(s): 2 Peritoneal exudate cells aggregate when exposed to the lymphokine, macrophage aggregating factor (MAgF). The role of prostaglandins in the aggregation of these cells was investigated. Prostaglandins E1, E2 and F2a did not cause aggregation by themselves, but they strongly inhibited the aggregation of macrophages induced by MAgF. The kinetics of aggregation induced by arachidonic acid differed from the kinetics of MAgF-induced aggregation. Aggregation induced by MAgF, the Ca ionophore A23187, and arachidonic acid was blocked by 5,8,11,14-eicosatetraynoic acid (an inhibitor of arachidonic acid metab.), by indomethacin (10-4, 10-6M), and by corticosteroids (dexamethasone, methylprednisolone, hydrocortisone), but not by aspirin (10-2, 10-4M) or phenylbutazone (10-4, 10-5M). These results suggest a causal relation between MAgF-induced macrophage aggregation and that due to other stimuli with respect to the derivs. of arachidonic acid. The lipoxygenase pathways metabolites stimulate aggregation, whereas the cyclo-oxygenase pathways metabolites inhibit it. .
In vitro characteristics of the lipid-filled interstitial cell associated with postnatal lung growth: evidence for fibroblast heterogeneity
In vitro characteristics of the lipid-filled interstitial cell associated with postnatal lung growth: evidence for fibroblast heterogeneity. Maksvytis, Harvey J.; Niles, Richard M.; Simanovsky, Leonid; Minassian, I. A.; Richardson, Laura L.; Hamosh, Margit; Hamosh, Paul; Brody, Jerome S. (Sch. Med., Boston Univ., Boston, MA 02118, USA). J. Cell. Physiol., 118(2), 113-23 (English) 1984. CODEN: JCLLAX. ISSN: 0021-9541. DOCUMENT TYPE: Journal CA Section: 13 (Mammalian Biochemistry) Section cross-reference(s): 2 In vitro modulation of the lipid-filled phenotype of lipid interstitial cells (LIC) isolated from the developing rat lung was studied. Isolated LIC lose their cytoplasmic lipid droplets when cultured in fetal bovine serum (FBS) but retain their potential for lipid storage, since they rapidly reaccumulate lipid when subcultured in neonatal rat serum (NRS) or (to a lesser extent) in adult rat serum (ARS). The return of LIC to a lipid-filled state may not represent cell differentiation, since it occurs in the presence of bromodeoxyuridine. NRS contains 2-fold the concn. of free fatty acids of FBS or ARS. Doubling the free fatty acid concn. of FBS and ARS increases LIC storage lipids. The serum triglyceride concn. in ARS is 10-fold, and that in NRS is 23-fold, that in FBS. Since LIC lipoprotein lipase (LPL) activity is comparable to that found in 3T3-L1 adipocytes (0.56 vs. 1.72 units/mg DNA), the LIC have the potential of incorporating serum lipoprotein-triglyceride. The LPL activity of LIC is 9-12-fold that of fetal and adult rat lung fibroblasts and 50-fold that of human lung, trachea, or skin fibroblasts; LIC are probably a source of endothelial LPL in the developing lung. The response of LIC and adult rat lung fibroblast (ARLF) cAMP to hormones known to influence lipid synthesis or degrdn. shows that: only LIC respond to glucagon; PGE1 is a more potent stimulus to LIC; isoproterenol is a more potent stimulus to ARLF; and neither cell responds to ACTH.Except for chemicals metioned above, 7683-59-2 and 745-65-3 are also used. The unique nature of LIC supports the concept of fibroblast heterogeneity within tissues. .
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