Detail of "103429-31-8"
- MSDS Download

- CAS Number:
- 103429-31-8
- Name:
L-Threoninamide,D-phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-ornithyl-L-threonyl-3-mercapto-L-valyl-,cyclic (2®7)-disulfide
- Molecular Structure:

- Formula:
- C50H67 N11 O11 S2
- Molecular Weight:
- 1062.26
- Synonyms:
- 1,2-Dithia-5,8,11,14,17-pentaazacycloeicosane,cyclic peptide deriv.; CTOP
- Density:
- 1.42g/cm3
- Boiling Point:
- 1491.2°Cat760mmHg
- Flash Point:
- 855.7°C
- Safety:
WGK Germany 3
Details

L-Threoninamide,D-phenylalanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-ornithyl-L-threonyl-3-mercapto-L-valyl-,cyclic (2®7)-disulfide

| WGK Germany | 3 |
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Reference
- Effect of opioid receptor antagonists on vasodilator nerve actions in the perfused rat mesentery
- Effect of opioid receptor antagonists on vasodilator nerve actions in the perfused rat mesentery. Li, Yuanjian; Duckles, Sue Pier (Coll. Med.In this study,103429-31-8 is also used., Univ. California, Irvine, CA 92717, USA). Eur. J. Pharmacol., 204(3), 323-8 (English) 1991. CODEN: EJPHAZ. ISSN: 0014-2999. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Previous work suggests that opioid peptides modulate sensory nerves in the perfused rat mesentery. Therefore the hypothesis was tested that opioids are involved in the ongoing regulation of sensory nerve activity using selective opioid receptor antagonists. In the presence of guanethidine and methoxamine, transmural nerve stimulation caused a vasodilator response which was potentiated by naloxone (3 ′ 10-7M). However, naloxone did not affect vasodilator responses to exogenous calcitonin gene-related peptide. IC1 174864 (3 ′ 10-7M), a selective d receptor antagonist, had no effect on vasodilator responses to transmural nerve stimulation. In contrast D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH2 (3 ′ 10-7M), a selective m receptor antagonist, inhibited vasodilator responses to transmural nerve stimulation, effects which were abolished by naloxone treatment. In prepns. pretreated with b-funaltrexamine-HCl, an irreversible m receptor antagonist, naloxone no longer potentiated vasodilator responses to transmural nerve stimulation. These results suggest that potentiation of vasodilator responses to transmural nerve stimulation by naloxone may be due to blockade of m receptors, resulting in a reduced inhibitory modulation by endogenous opioids. These findings support the contention that prejunctional opioid receptors on sensory nerves may play a role in modulating activity of the cardiovascular system. .

