Gap19
目录号 : GC17681
Gap19 (KQIEIKKFK) 阻断 HC 但不阻断 GJC，并且特定于 Cx43。
Cas No.:1507930-57-5
Sample solution is provided at 25 µL, 10mM.
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Gap19 (KQIEIKKFK) blocks HCs but not GJCs and is specific for Cx43. Gap19 may resist myocardial ischemic injury[2]. Gap19 has a bimodal effect on Cx43 HC gating, decreasing gating to the fully open state while increasing substate gating, suggesting that Gap19 acts like a gating modifier on Cx43 HC.Gap19 disrupts the CT-CL interaction, thus making hc difficult to open[7].
Gap19, as a nonapeptide derived from the cytoplasmic loop of Cx43, inhibits astroglial Cx43 hemichannels in a dose-dependent manner, without affecting gap junction channels. This peptide, which not only selectively inhibits hemichannels but is also specific for Cx43[5].
When investigated the role of Gap19 on cerebral ischemia/reperfusion (I/R) injury in a mouse model of middle cerebral artery occlusion (MCAO). Ventricle-injected Gap19 significantly alleviated infarct volume, neuronal cell damage and neurological deficits after ischemia, the neuroprotective effect of Gap19 was significant stronger than Gap26. Post-treatment with TAT-Gap19 still provided neuroprotection when it was administered intraperitoneally at 4 h after reperfusion[1]. Gap19 exerted a neuroprotective effect after stroke via inhibition of the TLR4-mediated signaling pathway[4]. Treatment with Gap19 prevented metabolic inhibition-enhanced hemichannel openings, protected cardiomyocytes against volume overload and cell death following ischemia/reperfusion in vitro and modestly decreased the infarct size after myocardial ischemia/reperfusion in mice in vivo[3]. Intra-TG injection of the mimetic peptide GAP19, which inhibits Cx43 hemichannel formation, greatly reduced TMJ-evoked MMemg activity in all CFA-inflamed groups, while activity in sham groups was not affected[6].
References:
[1]. Chen B, Yang L, et,al. Inhibition of Connexin43 hemichannels with Gap19 protects cerebral ischemia/reperfusion injury via the JAK2/STAT3 pathway in mice. Brain Res Bull. 2019 Mar;146:124-135. doi: 10.1016/j.brainresbull.2018.12.009. Epub 2018 Dec 26. PMID: 30593877.
[2]. Wang JP, Yang ZT, et,al. L-carnosine inhibits neuronal cell apoptosis through signal transducer and activator of transcription 3 signaling pathway after acute focal cerebral ischemia. Brain Res. 2013 Apr 24;1507:125-33. doi: 10.1016/j.brainres.2013.02.032. Epub 2013 Feb 27. PMID: 23454231.
[3]. Wang N, De Vuyst E, et,al. Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury. Basic Res Cardiol. 2013 Jan;108(1):309. doi: 10.1007/s00395-012-0309-x. Epub 2012 Nov 8. PMID: 23184389; PMCID: PMC3666173.
[4]. Chen Y, Wang L, et,al. Inhibition of Connexin 43 Hemichannels Alleviates Cerebral Ischemia/Reperfusion Injury via the TLR4 Signaling Pathway. Front Cell Neurosci. 2018 Oct 17;12:372. doi: 10.3389/fncel.2018.00372. PMID: 30386214; PMCID: PMC6199357.
[5]. Abudara V, Bechberger J, et,al. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes. Front Cell Neurosci. 2014 Oct 21;8:306. doi: 10.3389/fncel.2014.00306. PMID: 25374505; PMCID: PMC4204617.
[6]. Ahmed F, Rahman M, et,al. Role of Connexin 43 in an Inflammatory Model for TMJ Hyperalgesia. Front Pain Res (Lausanne). 2021 Aug 3;2:715871. doi: 10.3389/fpain.2021.715871. PMID: 35295418; PMCID: PMC8915650.
[7]. Lissoni A, Wang N, et,al. Gap19, a Cx43 Hemichannel Inhibitor, Acts as a Gating Modifier That Decreases Main State Opening While Increasing Substate Gating. Int J Mol Sci. 2020 Oct 5;21(19):7340. doi: 10.3390/ijms21197340. PMID: 33027889; PMCID: PMC7583728.
| Cell experiment [1]: | |
|
Cell lines |
Astrocyte cell |
|
Preparation Method |
Concentration-dependent inhibition by Gap19 (30 min pre-incubation) of ATP release in cultured cortical astrocytes triggered by glutamate. |
|
Reaction Conditions |
0-104uM Gap19 for 30 min |
|
Applications |
Gap19 (30 min treatment) inhibited glutamate-triggered ATP release (Figure 2A).Etd+ uptake was inhibited in the presence of Gap19 in a dose-dependent manner, with the peptide applied prior to (30 min) and during Etd+ uptake.Gap19 was without any effect on gap junctional communication in astrocytes which in culture express only Cx43. |
| Animal experiment [2]: | |
|
Animal models |
Male ICR mice (25-30 g) |
|
Preparation Method |
Animals were randomly divided into different groups as follows: (I) vehicle group (sham); (II) Gap19 treated vehicle group (Gap19 group); (III) I/R group; (IV) Gap26 treated I/R group (I/R + Gap26 group); (V) Gap19 treated I/R group (I/R + Gap19 group).10 µg Gap19/Gap26 in 10 µl ddH2O was injected in lateral ventricle (300 µg/kg body weight, i.c.v.). TAT-Gap19 was administered at a dose of 25 mg/kg body weight (i.p.) in the post-treatment groups. |
|
Dosage form |
10 µg Gap19 |
|
Applications |
When investigated the role of Gap19 on cerebral ischemia/reperfusion (I/R) injury in a mouse model of middle cerebral artery occlusion (MCAO). Ventricle-injected Gap19 significantly alleviated infarct volume, neuronal cell damage and neurological deficits after ischemia, the neuroprotective effect of Gap19 was significant stronger than Gap26. Post-treatment with TAT-Gap19 still provided neuroprotection when it was administered intraperitoneally at 4 h after reperfusion. |
|
References: [1]. Abudara V, Bechberger J, et,al. The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes. Front Cell Neurosci. 2014 Oct 21;8:306. doi: 10.3389/fncel.2014.00306. PMID: 25374505; PMCID: PMC4204617. | |
| Cas No. | 1507930-57-5 | SDF | |
| Canonical SMILES | CC[C@]([C@@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](N)([H])CCCCN)([H])CCC(O)=N)([H])[C@@](CC)([H])C)([H])CCC(O)=O)([H])/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](C(O)=O)([H])CCCCN)([H])CC1=CC=CC=C1)([H])CCCCN)([H])CCCCN)([H])C | ||
| 分子式 | C55H96N14O13 | 分子量 | 1161.45 |
| 溶解度 | ≥ 58.0725mg/mL in Water | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.861 mL | 4.305 mL | 8.6099 mL |
| 5 mM | 0.1722 mL | 0.861 mL | 1.722 mL |
| 10 mM | 0.0861 mL | 0.4305 mL | 0.861 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet