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H-89 dihydrochloride

产品编号 T6250 CAS 130964-39-5

别名: H 89 2HCl, 5-Isoquinolinesulfonamide, Protein kinase inhibitor H-89 dihydrochloride

H-89 dihydrochloride 是一种选择性 cAMP 依赖性蛋白激酶A (PKA) 抑制剂，IC50值为 48 nM。也可轻微抑制 PKG、PKC 和酪蛋白激酶活性。

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H-89 dihydrochloride, CAS 130964-39-5

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纯度: 100%

纯度: 98.38%

纯度: 98.22%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	H 89 is a potent inhibitor of protein kinase A (PKA; IC50: 0.14 μM, Ki: 48 nM).
靶点活性	S6K1:80 nM (cell free), PKA:48 nM (Ki, cell free)
体外活性	H-89 was shown to have a potent and selective inhibitory action against protein kinase A, with Ki of 0.048 microM. Pretreatment with H-89 led to a dose-dependent inhibition of the forskolin-induced protein phosphorylation, with no decrease in intracellular cyclic AMP levels in PC12D cells, and the NGF-induced protein phosphorylation was not inhibited. H-89 also significantly inhibited the forskolin-induced neurite outgrowth from PC12D cells. This inhibition also occurred when H-89 was added before the addition of dibutyryl cAMP. Pretreatment of PC12D cells with H-89 (30 microM) inhibited significantly cAMP-dependent histone IIb phosphorylation activity in cell lysates but did not affect other protein phosphorylation activity [1]. H-89 also inhibits S6K1, MSK1, ROCK-II, PKBα, and MAPKAP-K1b with IC50 values of 0.08, 0.12, 0.27, 2.6, and 2.8 μM, respectively [2]. In skinned EDL fibers of the rat, force responses to depolarization (by ion substitution) were inhibited only slightly by 10 microM H-89, a concentration more than sufficient to fully inhibit PKA. At 1-2 microM, H-89 significantly slowed the repriming rate in rat skinned fibers. With 100 microM H-89, the force response to depolarization by ion substitution was completely abolished. In intact single fibers of the flexor digitorum longus (FDB) muscle of the mouse, 1-3 microM H-89 had no noticeable effect on action-potential-mediated Ca2+ transients [3].
体内活性	Different doses of H-89 (0.05, 0.1, 0.2 mg/100g) were administered intraperitoneally (i.p.), 30 min before intravenous (i.v.) infusion of PTZ (0.5% w/v). Intraperitoneal administration of H-89 (0.2 mg/100g) significantly increased seizure latency and threshold in PTZ-treated animals. Pretreatment of animals with PTX (50 and 100 mg/kg) attenuated the anticonvulsant effect of H-89 (0.2 mg/100g) in PTZ-exposed animals. H-89 (0.05, 0.2 mg/100g) prevented the epileptogenic activity of bucladesine (300 nM) with a significant increase of seizure latency and seizure threshold [4]. Treatment with H89 (10 mg/kg, administered i.p.) significantly inhibited AHR in OVA-sensitized/challenged mice, whereas it had no effect on airway responses in control mice. Treatment with H89 decreased eosinophil numbers by 80%, neutrophil numbers by 64% and lymphocyte numbers by 74% without any effect on macrophage. In the moderate model, the cell infiltrate consisted of 39.3% eosinophils, 58.5% macrophages, 1.9% neutrophils, and 0.3% lymphocytes and was entirely inhibited by H89 [5].
激酶实验	All protein kinase activities were linear with respect to time in every incubation. Assays were performed either manually for 10 min at 30 °C in 50 μl incubations using [γ-32P]ATP or with a Biomek 2000 Laboratory Automation Workstation in a 96-well format for 40 min at ambient temperature in 25 μl incubations using [γ-33P]ATP. The concentrations of ATP and magnesium acetate were 0.1 mM and 10 mM respectively unless stated otherwise. This concentration of ATP is 5–10-fold higher than the Km for ATP of most of the protein kinases studied in the present paper, but lower than the normal intracellular concentration, which is in the millimolar range. All assays were initiated with MgATP. Manual assays were terminated by spotting aliquots of each incubation on to phosphocellulose paper, followed by immersion in 50 mM phosphoric acid. Robotic assays were terminated by the addition of 5 μl of 0.5 M phosphoric acid before spotting aliquots on to P30 filter mats. All papers were then washed four times in 50 mM phosphoric acid to remove ATP, once in acetone (manual incubations) or methanol (robotic incubations), and then dried and counted for radioactivity [2].
细胞实验	After 48 h in culture, PCl2D cells are cultured in a test medium containing 30 μM H-89 for 1 h and then exposed to a fresh medium that contained both 10 μM forskolin and 30 μM H-89. Cells are scraped off with a rubber policeman and sonicated in the presence of 0.5 mL of 6% trichloroacetic acid. To extract trichloroacetic acid, 2 mL of petroleum ether is added, the preparation mixed and centrifuged at 3000 rpm for 10 min. After aspiration of the upper layer, the residue sample solution is used for determination [1].
动物实验	H89 (N-[2-(p-Bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide], di-HCl Salt) (10 mg/kg) suspended in 5% DMSO in saline was administered i.p. two hours before each OVA challenge (or two hours before the last OVA challenge). Control animals received equivalent volumes (200 μl) of 5% DMSO in saline [5].

别名	H 89 2HCl, 5-Isoquinolinesulfonamide, Protein kinase inhibitor H-89 dihydrochloride
分子量	519.28
分子式	C20H20BrN3O2S·2HCl
CAS No.	130964-39-5

存储

Powder: -20°C for 3 years | In solvent: -80°C for 2 years

溶解度

H2O: 10 mg/mL (19 mM)

DMSO: 51.9 mg/mL (100 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )

参考文献

1. Chijiwa T, et al. Inhibition of forskolin-induced neurite outgrowth and protein phosphorylation by a newly synthesized selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), of PC12D pheochromocytoma cells. J Biol Chem. 1990 Mar 25;265(9):5267-72. 2. Davies SP, et al. Specificity and mechanism of action of some commonly used protein kinase inhibitors. Biochem J. 2000 Oct 1;351(Pt 1):95-105. 3. Blazev R, et al. Effects of the PKA inhibitor H-89 on excitation-contraction coupling in skinned and intact skeletal muscle fibres. J Muscle Res Cell Motil. 2001;22(3):277-86. 4. Hosseini-Zare MS, et al. Effects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice. Eur J Pharmacol. 2011 Nov 30;670(2-3):464-70. 5. Reber LL, et al. The AGC kinase inhibitor H89 attenuates airway inflammation in mouse models of asthma. PLoS One. 2012;7(11):e49512. 6. Liu M, Yang Y, Tan B, et al. Gαi and Gβγ subunits have opposing effects on dexmedetomidine-induced sedation[J]. European journal of pharmacology. 2018 Jul 15;831:28-37. 7. Xu C, Zhao W, Huang X, et al. TORC2/3-mediated DUSP1 upregulation is essential for human decidualization[J]. Reproduction. 2021, 1(aop). 8. Fu T, Chai B, Shi Y, et al. Fargesin inhibits melanin synthesis in murine malignant and immortalized melanocytes by regulating PKA/CREB and P38/MAPK signaling pathways[J]. Journal of Dermatological Science. 2019 Mar 28. pii: S0923-1811(19)30069-6.

文献引用

1. Han J, Wang Y, Qiu Y, et al. Single-cell sequencing unveils key contributions of immune cell populations in cancer-associated adipose wasting. Cell Discovery. 2022, 8(1): 1-22. 2. Zhang, Hongyan, et al. Intracellular AGR2 transduces PGE2 stimuli to promote epithelial–mesenchymal transition and metastasis of colorectal cancer.. Cancer Letters. 2021 3. Pan H, Lin Y, Dou J, et al. Wedelolactone facilitates Ser/Thr phosphorylation of NLRP3 dependent on PKA signalling to block inflammasome activation and pyroptosis. Cell Proliferation. 2020, 53(9): e12868 4. Fu T, Chai B, Shi Y, et al. Fargesin inhibits melanin synthesis in murine malignant and immortalized melanocytes by regulating PKA/CREB and P38/MAPK signaling pathways. Journal of Dermatological Science. 2019 Mar 28. pii: S0923-1811(19)30069-6. 5. Xu C, Zhao W, Huang X, et al. TORC2/3-mediated DUSP1 upregulation is essential for human decidualization. Reproduction. 2021, 1(aop). 6. Liu M, Yang Y, Tan B, et al. Gαi and Gβγ subunits have opposing effects on dexmedetomidine-induced sedation. European Journal of Pharmacology. 2018 Jul 15;831:28-37 7. Meng Y, Li W, Hu C, et al.Ginsenoside F1 administration promotes UCP1-dependent fat browning and ameliorates obesity-associated insulin resistance.Food Science and Human Wellness.2023, 12(6): 2061-2072. 8. Zhao W, Xu C, Peng L, et al.cAMP/PKA signaling promotes AKT deactivation by reducing CIP2A expression, thereby facilitating decidualization.Molecular and Cellular Endocrinology.2023: 111946. 9. Shan G, Bi G, Zhao G, et al.Inhibition of PKA/CREB1 pathway confers sensitivity to ferroptosis in non-small cell lung cancer.Respiratory Research.2023, 24(1): 1-15. 10. Cui S, Suo N, Yang Y, et al.The aminosteroid U73122 promotes oligodendrocytes generation and myelin formation.Acta Pharmacologica Sinica.2023: 1-12.

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

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分子量

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容积 (起始)

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配液浓度

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技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

H-89 dihydrochloride 130964-39-5 Autophagy MAPK PI3K/Akt/mTOR signaling Tyrosine Kinase/Adaptors PKA S6 Kinase Inhibitor inhibit H 89 2HCl H 89 dihydrochloride Protein kinase A H89 5-Isoquinolinesulfonamide H89 dihydrochloride Protein kinase inhibitor H-89 dihydrochloride H-89 H 89 inhibitor

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H-89 dihydrochloride

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