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H-89 dihydrochloride

カタログ番号 T6250   CAS 130964-39-5
別名: Protein kinase inhibitor H-89 dihydrochloride, H 89 2HCl, 5-Isoquinolinesulfonamide

H-89 dihydrochloride (5-Isoquinolinesulfonamide) is a potent inhibitor of protein kinase A (PKA; IC50: 0.14 μM, Ki: 48 nM).

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H-89 dihydrochloride, CAS 130964-39-5
パッケージサイズ 在庫状況 単価(税別)
無料サンプル 1 mg
5 mg 在庫あり ¥ 7,500
10 mg 在庫あり ¥ 12,500
25 mg 在庫あり ¥ 25,000
50 mg 在庫あり ¥ 49,000
100 mg 在庫あり ¥ 83,500
200 mg 在庫あり ¥ 123,500
500 mg 在庫あり ¥ 197,000
1 mL * 10 mM (in DMSO) 在庫あり ¥ 11,000
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生物学的特性に関する説明
化学的特性
保存条件 & 溶解度情報
説明 H-89 dihydrochloride (5-Isoquinolinesulfonamide) is a potent inhibitor of protein kinase A (PKA; IC50: 0.14 μM, Ki: 48 nM).
ターゲット&IC50 S6K1:80 nM (cell free), PKA:48 nM (Ki, cell free)
In vitro 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].
In vivo 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].
キナーゼ試験 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].
細胞研究 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].
動物実験 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].
別名 Protein kinase inhibitor H-89 dihydrochloride, H 89 2HCl, 5-Isoquinolinesulfonamide
分子量 519.28
分子式 C20H20BrN3O2S·2HCl
CAS No. 130964-39-5

保存条件

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度情報

H2O: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 51.9 mg/mL (100 mM)

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.

引用文献

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.
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投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください
投与量
mg/kg
動物の平均体重
g
動物あたりの投与量
ul
動物数
溶媒の組成を入力してください
% DMSO
%
% Tween 80
% ddH2O
計算する リセット

計算器

モル濃度計算機
希釈計算機
再構成計算
分子量計算機
=
X
X

モル度計算機では以下の計算が可能です

  • 既知の体積と濃度の溶液を調製するために必要な化合物の質量
  • 質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
  • 特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度
参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか?
[分子量(MW)]の欄に[197.13]と入力してください
[濃度]ボックスに10と入力し、正しい単位(millimolar)を選択します
[容量]ボックスに10と入力し、正しい単位(milliliter)を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

X
=
X

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2&V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか?
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度(開始)ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度(終了)ボックスに50を入力し正しい単位(millimolar)を選択してください
体積(終了)ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積(開始)ボックスに表示されます。

=
/

バイアルを再構成するのに必要な溶媒の量を計算する.

再構成計算機を使えば、バイアルを再構成するための試薬の量をすぐに計算することができます.
試薬の質量と目標濃度を入力するだけで計算します。

g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント:化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量(分子量)を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量(分子量)とは、物質の1分子の質量であり、統一された原子質量単位(u)で表されます。(1uは炭素12の1原子の質量の1/12に等しい)
モル質量(molar weight)とは、ある物質の1モルの質量のことで、単位はg/molです。

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技術サポート

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.

Keywords

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