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Gap 26Gap junction blocker peptide, mapping to connexin 43 residue 63-75

Gap 26

Catalog No. BCC1032
Size Price Stock
5mg $135.00 In stock
10mg $225.00 In stock
25mg $315.00 In stock
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Quality Control of Gap 26

Chemical structure

Gap 26


Cell experiment: [1]

Cell lines

ECV304 cells

Preparation method

The solubility of this peptide in sterile water is >10 mM. Stock solution should be splited and stored at -80°C for several months.

Reacting condition

0.25mg/ml, 30min


Preventing the InsP3-triggered calcium increase by ester loading the cells with the calcium chelator BAPTA reduced the InsP3-triggered ATP release back to the control level. Incubation of the cells with gap 26 completely abolished the InsP3-triggered ATP response and reduced the ATP release to below the control level, indicating that the basal ATP release is also affected.

Animal experiment: [2]

Animal models

Female Sprague-Dawley rats

Dosage form

300 μM, 45 min


The rats were prepared with closed cranial windows 24 h before the study. A 10-mm-diameter craniotomy was performed over the skull midline. The dura was removed carefully to keep the sagittal sinus intact. An 11-mm-diameter glass window outfitted with three ports was glued to the skull using cyanoacrylate. The skin overlying the window was sutured, and the animals were permitted to recover. On the day of study, three stainless steel screws were inserted into the skull, along the periphery of the cranial window, for electroencephalogram (EEG) recording. Cannulae were then connected to the three ports. The rats were subjected to one of two neuronal activation paradigms: SNS or bicuculline-induced seizure. Following the initial measurement of pial arteriolar diameter changes during SNS or during bicuculline exposure, baseline conditions were reestablished. After 20 min, a suffusion of gap-26 was initiated. Forty-five minutes later, the neural activation was repeated. Exposure to the Cx40/Cx37 inhibitory peptide, gap-26 (300 μM), was without effect on bicuculline- or SNS-induced pial arteriolar dilations.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Braet K, Vandamme W, Martin P E M, et al. Photoliberating inositol-1, 4, 5-trisphosphate triggers ATP release that is blocked by the connexin mimetic peptide gap 26. Cell calcium, 2003, 33(1): 37-48.

[2] Xu H L, Mao L, Ye S, et al. Astrocytes are a key conduit for upstream signaling of vasodilation during cerebral cortical neuronal activation in vivo. American Journal of Physiology-Heart and Circulatory Physiology, 2008, 294(2): H622-H632.

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Chemical Properties of Gap 26

Cas No. 197250-15-0 SDF Download SDF
Chemical Name (2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2R)-2-[[(2S)-2-amino-3-methylbutanoyl]amino]-3-sulfanylpropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]-3-hydroxypropanoyl]amino]-3-phenylpropanoyl]pyrrolidine-2-carbonyl]amino]-3-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-3-methylbutanoyl]amino]-5-(diaminomethylideneamino)pentanoic acid
SMILES [H]/N=C(N)/NCCC[C@@H](C(=O)O)NC(=O)[C@H](C(C)C)NC(=O)[C@H](Cc1cnc[nH]1)NC(=O)[C@H](CO)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@@H]2CCCN2C(=O)[C@H](Cc3ccccc3)NC(=O)[C@H](CO)NC(=O)[C@H](CCCCN)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](Cc4ccc(cc4)O)NC(=O)[C@H](CS)NC(=O)[C@H](C(C)C)N
Standard InChI InChI=1S/C70H107N19O19S/c1-7-38(6)56(67(105)85-50(33-91)61(99)81-46(29-41-31-75-35-77-41)60(98)87-55(37(4)5)66(104)79-44(69(107)108)18-13-25-76-70(73)74)88-64(102)52-19-14-26-89(52)68(106)48(28-39-15-9-8-10-16-39)83-62(100)49(32-90)84-57(95)43(17-11-12-24-71)78-59(97)47(30-53(93)94)82-58(96)45(27-40-20-22-42(92)23-21-40)80-63(101)51(34-109)86-65(103)54(72)36(2)3/h8-10,15-16,20-23,31,35-38,43-52,54-56,90-92,109H,7,11-14,17-19,24-30,32-34,71-72H2,1-6H3,(H,75,77)(H,78,97)(H,79,104)(H,80,101)(H,81,99)(H,82,96)(H,83,100)(H,84,95)(H,85,105)(H,86,103)(H,87,98)(H,88,102)(H,93,94)(H,107,108)(H4,73,74,76)/t38-,43-,44-,45-,46-,47-,48-,49-,50-,51-,52-,54-,55-,56-/m0/s1
Formula C70H107N19O19S M.Wt 1550.79
Solubility Soluble to 2 mg/ml in water
Storage Desiccate at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Background on Gap 26

Gap26 (Val-Cys-Tyr-Asp-Lys-Ser-Phe-Pro-Ile-Ser-His-Val-Arg) is a connexin mimetic peptide, corresponding to residues 63-75 of connexin 43, which is a gap junction blocker.

Connexins, or gap junctions, are a family of structurally-related transmembrane proteins. Gap junctions contain channels that allow the passage of ions and small molecules between adjacent cells molecules. Calcium and inositol phosphates are among the second messengers that can pass through gap junction channels. [1] It was showed that gap26 attenuates rhythmic contractile activity of rabbit arterial smooth muscle (IC50 = 28.4 mM). It also blocks movement of IP3-induced ATP and Ca2+ across connexin hemichannels, i.e. hexameric channels yet to dock with partners in aligned cells and to generate the gap junction cell–cell conduit. [2]


Fig. 1: Formula of Gap26


Fig. 2: Function of Gap26.



1. Boitano, S. and H. Evans Am. J. Physiol. Lung Cell Mol. Physiol. 279, L623 (2000).

2. T. Desplantez, V. Verma, L. Leybaert, W.H. Evans, R. Weingart, Gap26, a connexin mimetic peptide, inhibits currents carried by connexin43 hemichannels and gap junction channels, Pharmacological Research, Volume 65, Issue 5, May 2012, Pages 546-552.

References on Gap 26

Bridging the Gap, Facing the Challenge-the 26(th) Great Wall International Congress of Cardiology (GW-ICC).[Pubmed: 26885499]

The joint venue of the 26(th) Great Wall International Congress of Cardiology (GW-ICC) & Asia Pacific Heart Congress 2015 (APHC 2015) & International Congress Cardiovascular Prevention and Rehabilitation 2015 (ICCPR 2015) were held from October 29 to November 01, 2015 at the China National Convention Center (CNCC), Beijing, China. This year's conference focused on cardiovascular disease prevention, health promotion, education and training, as well as disease management and rehabilitation.

Gap-junctional channel and hemichannel activity of two recently identified connexin 26 mutants associated with deafness.[Pubmed: 26769242]

Gap-junction channels (GJCs) are formed by head-to-head association of two hemichannels (HCs, connexin hexamers). HCs and GJCs are permeable to ions and hydrophilic molecules of up to Mr ~1 kDa. Hearing impairment of genetic origin is common, and mutations of connexin 26 (Cx26) are its major cause. We recently identified two novel Cx26 mutations in hearing-impaired subjects, L10P and G109V. L10P forms functional GJCs with slightly altered voltage dependence and HCs with decrease ATP/cationic dye selectivity. G109V does not form functional GJCs, but forms functional HCs with enhanced extracellular Ca(2+) sensitivity and subtle alterations in voltage dependence and ATP/cationic dye selectivity. Deafness associated with G109V could result from decreased GJCs activity, whereas deafness associated to L10P may have a more complex mechanism that involves changes in HC permeability.

[Expression of gap junction protein connexin 26 in human hepatocellular carcinoma and its significance].[Pubmed: 26713526]

To investigate the expression of gap junction protein connexin 26(Cx26) in hepatocellular carcinoma(HCC) and its significance.

Impaired gap junctions in human hepatocellular carcinoma limit intrinsic oxaliplatin chemosensitivity: A key role of connexin 26.[Pubmed: 26648344]

Hepatocellular carcinoma (HCC) is generally believed to have low sensitivity to chemotherapeutic agents including oxaliplatin (OXA). Studies have demonstrated that gap junctions (GJs) composed of connexin (Cx) proteins have the potential to modulate drug chemosensitivity in multiple tumor cells. In the present study, we investigated the characteristics of Cx and GJs in HCC at both histologic and cytologic levels, and the effects of GJ and its effective components on OXA cytotoxicity in HCC cells in vitro. Immunohistochemistry was performed in 76 HCCs and 20 normal liver tissues to detect and locate the expression of Cx26, Cx32 and Cx43. At cytologic levels, the expression and localization of Cxs were evaluated by RT-PCR, western blot and immunofluorescence assay, respectively. The GJ function between adjacent cells was detected using dye transfer assay. The role of GJs in the modulation of OXA toxicity in HCC cells was explored using pharmacologic and molecular biologic methods. We found that Cx expression in HCC tissues was significantly lower than in normal liver tissues, and the 'internalization' from cell membrane to cytoplasm was remarkable. In vitro experiments revealed the presence of functional GJs in the SMMC-7721 HCC cells due to a small amount of Cx protein along the plasma membrane at cell-cell contacts. Regulation of this part of GJs positively influenced OXA cytotoxicity. Using RNA interference, only specific inhibition of Cx26 but not Cx32 or Cx43 reduced OXA cytotoxicity. Conversely, Cx26 overexpression by transfection of Cx26 plasmid DNA enhanced OXA cytotoxicity. This study demonstrated that during hepatocarcinogenesis, the reduced expression and internalization of Cx proteins impaired the GJ function, which further attenuated OXA cytotoxicity. Impaired GJ function may contribute to low intrinsic chemosensitivity of HCC cells to OXA, mediated by Cx26.


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