Pinacidil monohydrate
(Synonyms: 吡那地尔一水合物; P-1134 monohydrate) 目录号 : GC30267
Pinacidil monohydrate一种抗高血压药物，属于钾通道开放剂，通过激活ATP敏感性钾通道使血管平滑肌松弛。
Cas No.:85371-64-8
Sample solution is provided at 25 µL, 10mM.
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Pinacidil monohydrate is an antihypertensive drug belonging to the class of potassium channel openers. Pinacidil monohydrate relaxes vascular smooth muscle by activating ATP-sensitive potassium channels[1-2]. Pinacidil monohydrate exhibits neuroprotective effects and improves blood lipid metabolism[3-4].
In vitro, treatment of HEK293T cells expressing SUR2B/Kir6.1 or SUR2B/Kir6.2 potassium channel complexes with Pinacidil monohydrate (100–300µM) for 24 hours, Pinacidil monohydrate significantly enhanced the activation of SUR2B/Kir6.1 channels by nucleotide di- or triphosphates (e.g., ATP, ADP, GTP, UDP). Pinacidil monohydrate was achieved by increasing the efficacy of nucleotides on slow gating mechanisms, thereby augmenting the number of functional channels[5]. Treatment of HepG2 human hepatoma cells with Pinacidil monohydrate (1mM) for 48 hours induced an increase in intracellular K⁺ and Na⁺ concentrations via activation of the Na⁺, K⁺, Cl⁻ cotransporter (NKCC). Pinacidil monohydrate led to a sustained rise in intracellular Ca²⁺ concentration through reverse activation of the Na⁺/Ca²⁺ exchanger, ultimately resulting in apoptosis[6].
In vivo, pretreatment of rats via intraperitoneal injection with Pinacidil monohydrate (10–50μg/kg) before skin/muscle incision and retraction (SMIR) surgery, Pinacidil monohydrate significantly inhibited the decrease in microvessel density (MVD) and glucose transporter-1 (GLUT1) expression in the peri-incisional microenvironment[7]. Pretreatment of C57BL/6J mice via intraperitoneal injection with Pinacidil monohydrate (0.1–0.5mg/kg/day) for three days prior to myocardial ischemia-reperfusion (I/R) injury, Pinacidil monohydrate significantly improved cardiac function, increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), and reduced serum BNP levels[8].
References:
[1] Ahnfelt-Rønne I. Pinacidil. Preclinical investigations. Drugs. 1988;36 Suppl 7:4-9.
[2] Friedel HA, Brogden RN. Pinacidil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the treatment of hypertension. Drugs. 1990 Jun;39(6):929-67.
[3] Pereira AT, Gelfuso ÉA, Beleboni RO. Repositioning pinacidil and its anticonvulsant and anxiolytic properties in murine models. Sci Rep. 2024 Sep 30;14(1):22695.
[4] Shukry M, Kamal T, Ali R, et al. Pinacidil and levamisole prevent glutamate-induced death of hippocampal neuronal cells through reducing ROS production. Neurol Res. 2015 Oct;37(10):916-23.
[5] Satoh E, Yamada M, Kondo C, et al. Intracellular nucleotide-mediated gating of SUR/Kir6.0 complex potassium channels expressed in a mammalian cell line and its modification by pinacidil. J Physiol. 1998 Sep 15;511 ( Pt 3)(Pt 3):663-74.
[6] Kim JA, Kang YY, Lee YS. Activation of Na(+), K(+), Cl(-)-cotransport mediates intracellular Ca(2+) increase and apoptosis induced by Pinacidil in HepG2 human hepatoblastoma cells. Biochem Biophys Res Commun. 2001 Feb 23;281(2):511-9.
[7] Cao S, Qin Y, Chen J, et al. Effects of pinacidil on changes to the microenvironment around the incision site, of a skin/muscle incision and retraction, in a rat model of postoperative pain. Mol Med Rep. 2015 Jul;12(1):829-36.
[8] Liu M, Li S, Yin M, et al. Pinacidil ameliorates cardiac microvascular ischemia-reperfusion injury by inhibiting chaperone-mediated autophagy of calreticulin. Basic Res Cardiol. 2024 Feb;119(1):113-131.
Pinacidil monohydrate一种抗高血压药物，属于钾通道开放剂，通过激活ATP敏感性钾通道使血管平滑肌松弛[1-2]。Pinacidil monohydrate具有保护神经系统，及改善血脂代谢作用[3-4]。
在体外，Pinacidil monohydrate（100–300µM）处理表达SUR2B/Kir6.1或SUR2B/Kir6.2复合钾通道的HEK293T细胞24h，显著增强核苷酸二磷酸或三磷酸（如ATP、ADP、GTP、UDP）对SUR2B/Kir6.1通道的激活作用，并通过提高核苷酸对慢门控机制的效能增加功能通道数量[5]。Pinacidil monohydrate（1mM）处理HepG2人肝癌细胞48小时，通过激活Na⁺，K⁺，Cl⁻共转运体（NKCC）诱导细胞内K⁺浓度和Na⁺浓度升高，通过反向激活Na⁺/Ca²⁺交换体引起细胞内Ca²⁺浓度持续增加，最终导致细胞凋亡[6]。
在体内，Pinacidil monohydrate（10–50μg/kg）于皮肤/肌肉切开牵拉术（SMIR）前腹腔注射预处理大鼠，显著抑制术后切口周围微环境中的微血管密度（MVD）下降和葡萄糖转运蛋白-1（GLUT1）表达减少[7]。Pinacidil monohydrate（0.1–0.5mg/kg/day）于心肌缺血再灌注（I/R）损伤前3天腹腔注射预处理C57BL/6J小鼠，显著改善心脏功能，提高左室射血分数（LVEF）和左室短轴缩短率（LVFS），并降低血清BNP水平[8]。
| Cell experiment [1]: | |
Cell lines | HepG2 human hepatoblastoma cells |
Preparation Method | HepG2 cells were maintained in Eagle’s Minimum Essential Medium (MEM) supplemented with 10% fetal bovine serum (FBS), 1mM sodium pyruvate, and antibiotics (200IU/mL penicillin, 200μg/mL streptomycin) at 37°C under 5% CO₂. Cells were treated with Pinacidil monohydrate (1mM) for 48 hours. |
Reaction Conditions | 1mM; 48h |
Applications | Pinacidil monohydrate significantly increased intracellular K⁺ and Na⁺ concentrations via activation of Na⁺,K⁺,Cl⁻-cotransport (NKCC), leading to a sustained rise in intracellular Ca²⁺ levels through reverse-mode Na⁺/Ca²⁺ exchanger activation. This Ca²⁺ surge induced apoptosis, characterized by DNA fragmentation, phosphatidylserine externalization, and hypodiploid DNA content. NKCC inhibitors (bumetanide, furosemide) or Ca²⁺ chelators (BAPTA/AM, EGTA) abolished these effects. |
| Animal experiment [2]: | |
Animal models | C57BL/6 mice |
Preparation Method | Mice were intraperitoneally administered Pinacidil monohydrate (0.1 or 0.5mg/kg/day) for 3 days prior to ischemia-reperfusion (I/R) injury induction. I/R injury was induced by ligating the left anterior descending coronary artery (LAD) for 45 minutes followed by reperfusion. Cardiac function and microvascular integrity were assessed 3 days post-I/R. |
Dosage form | 0.1–0.5mg/kg/day; i.p.; 3-day pretreatment |
Applications | Pinacidil monohydrate administration significantly improved cardiac function by increasing left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), and reduced infarct size by 40% compared to the I/R group. |
References: | |
| Cas No. | 85371-64-8 | SDF | |
| 别名 | 吡那地尔一水合物; P-1134 monohydrate | ||
| Canonical SMILES | [H]O[H].CC(C)(C)C(N/C(NC#N)=N/C1=CC=NC=C1)C | ||
| 分子式 | C13H21N5O | 分子量 | 263.34 |
| 溶解度 | 50 mg/ml in Ethanol (Need ultrasonic); 50 mg/ml in DMSO (Need ultrasonic) | 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.7974 mL | 18.9869 mL | 37.9737 mL |
| 5 mM | 759.5 μL | 3.7974 mL | 7.5947 mL |
| 10 mM | 379.7 μL | 1.8987 mL | 3.7974 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
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- Purity: >98.00%
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