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CTAP trifluoroacetate salt

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

CTAP is a water-soluble and selective antagonist of the µ opioid receptor (IC50 = 3.5 nM) over the δ receptor (IC50 = 4,500 nM). It is a cyclic octapeptide which acts as a poor antagonist of the somatostatin receptor (IC50 = 14.3 μM). CTAP is at least 10-fold more potent than naltrexone.

Category

Peptide Inhibitors

Catalog number

BAT-016434

Molecular Formula

C51H69N13O11S2·xCF3COOH

Molecular Weight

1104.31

Specification
Reference Reading

Related CAS

103429-32-9

Appearance

Solid Powder

InChI

InChI=1S/C51H69N13O11S2.C2HF3O2/c1-26(65)39(42(53)68)62-49(75)41-51(3,4)77-76-25-38(61-43(69)33(52)21-28-11-6-5-7-12-28)47(73)59-36(22-29-16-18-31(67)19-17-29)45(71)60-37(23-30-24-57-34-14-9-8-13-32(30)34)46(72)58-35(15-10-20-56-50(54)55)44(70)63-40(27(2)66)48(74)64-41;3-2(4,5)1(6)7/h5-9,11-14,16-19,24,26-27,33,35-41,57,65-67H,10,15,20-23,25,52H2,1-4H3,(H2,53,68)(H,58,72)(H,59,73)(H,60,71)(H,61,69)(H,62,75)(H,63,70)(H,64,74)(H4,54,55,56);(H,6,7)/t26-,27-,33-,35+,36+,37-,38+,39+,40+,41-;/m1./s1

InChI Key

OCNOBNFWFKDFMD-XQGGKHMTSA-N

Canonical SMILES

O=C([C@@H](CC1=CNC2=C1C=CC=C2)NC([C@H](CC3=CC=C(C=C3)O)NC([C@@H](NC([C@@H](CC4=CC=CC=C4)N)=O)CSSC(C)([C@H](NC5=O)C(N[C@@H]([C@@H](C)O)C(N)=O)=O)C)=O)=O)N[C@@H](CCCNC(N)=N)C(N[C@H]5[C@@H](C)O)=O.FC(F)(C(O)=O)F

1. Peripheral effects of morphine and expression of μ-opioid receptors in the dorsal root ganglia during neuropathic pain: nitric oxide signaling

Arnau Hervera, Olga Pol, Roger Negrete, Jesús M Martín-Campos, Sergi Leánez Mol Pain . 2011 Apr 12;7:25. doi: 10.1186/1744-8069-7-25.

Background:The local administration of μ-opioid receptor (MOR) agonists attenuates neuropathic pain but the precise mechanism implicated in this effect is not completely elucidated. We investigated if nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric oxide synthases could modulate the local antiallodynic effects of morphine through the peripheral nitric oxide-cGMP-protein kinase G (PKG)-ATP-sensitive K+ (KATP) channels signaling pathway activation and affect the dorsal root ganglia MOR expression during neuropathic pain.Results:In wild type (WT) mice, the subplantar administration of morphine dose-dependently decreased the mechanical and thermal allodynia induced by the chronic constriction of the sciatic nerve (CCI), which effects were significantly diminished after their co-administration with different subanalgesic doses of a selective NOS1 (N-[(4S)-4-amino-5-[(2-aminoethyl)amino]pentyl]-N'-nitroguanidine tris(trifluoroacetate) salt; NANT), NOS2 (L-N(6)-(1-iminoethyl)-lysine; L-NIL), L-guanylate cyclase (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; ODQ), PKG ((Rp)-8-(para-chlorophenylthio)guanosine-3',5'-cyclic monophosphorothioate; Rp-8-pCPT-cGMPs) inhibitor or a KATP channel blocker (glibenclamide). The evaluation of the expression of MOR in the dorsal root ganglia from sham-operated and sciatic nerve-injured WT, NOS1 knockout (KO) and NOS2-KO mice at 21 days after surgery demonstrated that, although the basal mRNA and protein levels of MOR were similar between WT and both NOS-KO animals, nerve injury only decreased their expression in WT mice.Conclusions:These results suggest that the peripheral nitric oxide-cGMP-PKG-KATP signaling pathway activation participates in the local antiallodynic effects of morphine after sciatic nerve injury and that nitric oxide, synthesized by NOS1 and NOS2, is implicated in the dorsal root ganglia down-regulation of MOR during neuropathic pain.