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ZIP

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

ZIP is a cell-permeable inhibitor of protein kinase Mζ (PKMζ), which is a constitutively active and atypical PKC isozyme involved in LTP maintenance. ZIP selectively blocks PKMζ-induced synaptic potentiation in hippocampal slices in vitro. ZIP reverses late-phase LTP (IC50 = 1 - 2.5 μM) and produces persistent loss of 1-day-old spatial memory following central administration in vivo.

Category

Peptide Inhibitors

Catalog number

BAT-010281

CAS number

863987-12-6

Molecular Formula

C90H154N30O17

Molecular Weight

1928.37

Specification
Reference Reading

IUPAC Name

(2S)-2-[[(2S)-6-amino-2-[[(2S)-5-carbamimidamido-2-[[(2S)-2-[[(2S)-5-carbamimidamido-2-[[(2S)-5-carbamimidamido-2-[[(2S)-2-[[2-[[(2S)-5-carbamimidamido-2-[[(2S)-5-carbamimidamido-2-[[(2S)-3-(4-hydroxyphenyl)-2-[[(2S,3S)-2-[[(2S)-3-hydroxy-2-(tetradecanoylamino)propanoyl]amino]-3-methylpentanoyl]amino]propanoyl]amino]pentanoyl]amino]pentanoyl]amino]acetyl]amino]propanoyl]amino]pentanoyl]amino]pentanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]pentanoyl]amino]hexanoyl]amino]-4-methylpentanoic acid

Synonyms

ZIP; FLJ36473; DAPK3, active, GST tagged human; PKC Zeta Pseudosubstrate Inhibitory peptide; Protein kinase Cζ pseudosubstrate, myristoyl trifluoroacetate salt; N-(1-Oxotetradecyl)-L-seryl-L-isoleucyl-L-tyrosyl-L-arginyl-L-arginylglycyl-L-alanyl-L-arginyl-L-arginyl-L-tryptophyl-L-arginyl-L-lysyl-L-leucine

Density

1.39±0.1 g/cm3(Predicted)

Sequence

SIYRRGARRWRKL

Storage

Store at -20°C

InChI

InChI=1S/C90H154N30O17/c1-7-9-10-11-12-13-14-15-16-17-18-36-71(123)110-70(52-121)83(134)120-73(54(5)8-2)84(135)118-67(48-56-37-39-58(122)40-38-56)81(132)115-64(33-25-44-104-88(96)97)77(128)112-61(31-23-42-102-86(92)93)75(126)108-51-72(124)109-55(6)74(125)111-63(32-24-43-103-87(94)95)76(127)114-66(35-27-46-106-90(100)101)79(130)117-68(49-57-50-107-60-29-20-19-28-59(57)60)82(133)116-65(34-26-45-105-89(98)99)78(129)113-62(30-21-22-41-91)80(131)119-69(85(136)137)47-53(3)4/h19-20,28-29,37-40,50,53-55,61-70,73,107,121-122H,7-18,21-27,30-36,41-49,51-52,91H2,1-6H3,(H,108,126)(H,109,124)(H,110,123)(H,111,125)(H,112,128)(H,113,129)(H,114,127)(H,115,132)(H,116,133)(H,117,130)(H,118,135)(H,119,131)(H,120,134)(H,136,137)(H4,92,93,102)(H4,94,95,103)(H4,96,97,104)(H4,98,99,105)(H4,100,101,106)/t54-,55-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,73-/m0/s1

InChI Key

CRKARHQCXWSUMV-HOHDCHNJSA-N

Canonical SMILES

CCCCCCCCCCCCCC(=O)NC(CO)C(=O)NC(C(C)CC)C(=O)NC(CC1=CC=C(C=C1)O)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCCNC(=N)N)C(=O)NCC(=O)NC(C)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCCNC(=N)N)C(=O)NC(CC2=CNC3=CC=CC=C32)C(=O)NC(CCCNC(=N)N)C(=O)NC(CCCCN)C(=O)NC(CC(C)C)C(=O)O

1.Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain.

King T;Qu C;Okun A;Melemedjian OK;Mandell EK;Maskaykina IY;Navratilova E;Dussor GO;Ghosh S;Price TJ;Porreca F Pain. 2012 Jun;153(6):1263-73. doi: 10.1016/j.pain.2012.03.006. Epub 2012 Apr 4.

Injuries can induce adaptations in pain processing that result in amplification of signaling. One mechanism may be analogous to long-term potentiation and involve the atypical protein kinase C, PKMζ. The possible contribution of PKMζ-dependent and independent amplification mechanisms to experimental neuropathic pain was explored in rats with spinal nerve ligation (SNL) injury. SNL increased p-PKMζ in the rostral anterior cingulate cortex (rACC), a site that mediates, in part, the unpleasant aspects of pain. Inhibition of PKMζ within the rACC by a single administration of ζ-pseudosubstrate inhibitory peptide (ZIP) reversed SNL-induced aversiveness within 24 hours, whereas N-methyl-d-aspartate receptor blockade with MK-801 had no effects. The SNL-induced aversive state (reflecting "spontaneous" pain), was re-established in a time-dependent manner, with full recovery observed 7 days post-ZIP administration. Neither rACC ZIP nor MK-801 altered evoked responses. In contrast, spinal ZIP or MK-801, but not scrambled peptide, transiently reversed evoked hypersensitivity, but had no effect on nerve injury-induced spontaneous pain. PKMζ phosphorylation was not altered by SNL in the spinal dorsal horn.

2.Involvement of protein kinase ζ in the maintenance of hippocampal long-term potentiation in rats with chronic visceral hypersensitivity.

Chen A;Bao C;Tang Y;Luo X;Guo L;Liu B;Lin C J Neurophysiol. 2015 May 1;113(9):3047-55. doi: 10.1152/jn.00929.2014. Epub 2015 Mar 11.

The hippocampal long-term potentiation (LTP) was implicated in the formation of visceral hypersensitivity in rats with irritable bowel syndrome in our previous study. Recent studies have shown that protein kinase M ζ (PKMζ) may be responsible for the maintenance of LTP in memory formation. However, it remains unclear whether PKMζ is involved in the visceral hypersensitivity. In this study, a rat model of visceral hypersensitivity was generated by neonatal maternal separation (NMS). The visceral hypersensitivity was assessed by recording responses of the external oblique abdominal muscle to colorectal distension. Our results demonstrated that hippocampal LTP and visceral hypersensitivity were enhanced significantly in rats of NMS. ζ-Pseudosubstrate inhibitory peptide (ZIP) could dose dependently inhibit the maintenance of Cornu Ammonis area 1 LTP in rats of NMS. Furthermore, Western blot data showed that the expression of hippocampal phosphorylated PKMζ (p-PKMζ) significantly increased in rats of NMS. In addition, bilateral intrahippocampal injections of ZIP attenuated the visceral hypersensitivity dose dependently in rats of NMS. The maximal inhibition was observed at 30 min, and significant inhibition lasted for 1.