Pitavastatin (NK-104) calcium

For research use only. Not for use in humans.

製品コードS1759 別名:P-872441, itavastatin, nisvastatin

Pitavastatin (NK-104) calcium化学構造

CAS No. 147526-32-7

Pitavastatin Calcium (NK-104, P-872441, itavastatin, nisvastatin), a novel member of the medication class of statins, is a calcium salt formulation of pitavastatin which is a highly effective HMG-CoA reductase inhibitor. Pitavastatin Calcium attenuates AGEs-induced mitophagy via inhibition of ROS generation. Pitavastatin Calcium induces autophagy and apoptosis.

サイズ 価格(税別)  
JPY 18100
JPY 53400
JPY 109400
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バルク問合せ

カスタマーフィードバック(3)

  • Western blotting showed that in U87 cells treated with pitavastatin, the LC3-II isoform dramatically increased after statin treatment and showed at day 2, 3 and 4.

    Br J Cancer, 2014, 111(8): 1562-71 . Pitavastatin (NK-104) calcium purchased from Selleck.

    Fewer proliferative cells were detected in the tumour after pitavastatin treatment according to the Ki67 staining results but not in fluvastatin group.

    Br J Cancer, 2014, 111(8): 1562-71 . Pitavastatin (NK-104) calcium purchased from Selleck.

  • Western blot analysis of Nrf2, NQO1, and HO-1 in statin-treated VSMCs. Cells were exposed to fluvastatin and pitavastatin for 24 h at the indicated dosages. In addition, protein samples were refined from cultured VSMCs treated with fluvastatin (5 μM) or pitavastatin (5 μM) for the indicated times.

    PLoS One, 2017, 12(5):e0178278. Pitavastatin (NK-104) calcium purchased from Selleck.

製品安全説明書

HMG-CoA Reductase阻害剤の選択性比較

生物活性

製品説明 Pitavastatin Calcium (NK-104, P-872441, itavastatin, nisvastatin), a novel member of the medication class of statins, is a calcium salt formulation of pitavastatin which is a highly effective HMG-CoA reductase inhibitor. Pitavastatin Calcium attenuates AGEs-induced mitophagy via inhibition of ROS generation. Pitavastatin Calcium induces autophagy and apoptosis.
ターゲット
cholesterol esters [1] HMG-CoA reductase [4]
体外試験

Pitavastatin significantly reduces both intracellular levels and synthesis of cholesterol esters. Pitavastatin is found to enhance LDL-receptor expression in vitro, as well as the amount of LDL binding to the LDL-receptor. Pitavastatin also exhibits more potent induction of LDL receptor mRNA expression compared with simvastatin and atorvastatin. Pitavastatin has many pleiotropic effects in vitro and in vivo, including deterring progression of atherosclerosis via inhibition of thromboxane synthesis, inhibition of migration/proliferation of vascular smooth muscle cells induced by angiotensin II, and stabilization of atherosclerotic plaque. [1] Pitavastatin is able to activate PPARα and induce HDL apoA-I through inducing inhibition of the Rho-signaling pathway. [2] Pitavastatin (1 μM) treatment for 48 h is able to enhances bone morphogenetic protein-2 BMP-2 (2.5-fold) and osteocalcin (10-fold) expression by inhibition of Rho-associated kinase in human osteoblasts[3]. Pitavastatin inhibits growth and colony formation of liver cancer Huh-7 cells and SMMC7721 cells. It induces arrest of liver cancer cells at the G1 phase. Increased proportion of sub-G1 cells is observed after pitavastatin treatment. Pitavastatin promotes caspase-9 cleavage and caspase-3 cleavage in liver cancer cells. Pitavastatin could regulate NF-κB and anti-inflammation in hepatocellular carcinoma cells. Pitavastatin could induce autophagic cell death in glioma cells and promote sensitivity of cells to radiotherapy. It could inhibit cell proliferation and induce cell apoptosis in cholangiocarcinoma cells as well[5].

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 NVjRb2F[TnWwY4Tpc44h[XO|YYm= M{\kT2RzfWdidYD0ZYtmKGmwIFjFT|I6OyClZXzsd{BmgHC{ZYPzbY5oKE:DVGCxRlEhMHWwa37ve44hd3KrZ3nuLUBie3Onc4Pl[EBieyCRQWTQNWIyNW2nZHnheIVlKGS{dXegeJJidnOyb4L0MEBMdSB;IESuPEDPxE1w M{P3RlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{NUi3PVg3Lz5{MkW4O|k5PjxxYU6=
hepatocytes NVXK[XZzTnWwY4Tpc44h[XO|YYm= M4e3VFAvOSC2bzCxNEB2VQ>? Ml6yeZAhfG9iOUCgcYlvew>? MWPEdpVoKG2ndHHic4xqe21iaX6gV5Bz[We3ZT3EZZdt\XlicnH0JIhmeGG2b3P5eIV{KGG|c3Xzd4VlKHCncjCxNEc3KGOnbHzzJIF1KDBwMTD0c{AyOCC3TTD1dEB1dyB7MDDtbY5{KGK7IH3l[IliNWyxc4OgcYV1cG:mLDDLcUA:KDF|IN88UU4> MlXQQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjJ3OUOwN|goRjJ{NUmzNFM5RC:jPh?=
Neuro2a MkT4SpVv[3Srb36gZZN{[Xl? MmXFNUB2VQ>? MoDkTY5pcWKrdHnvckBw\iCmZXz0ZUA5NTdiaYPvcYVz[XOnIHnuJI1wfXOnIF7leZJwOmFiY3XscJMh[XO|ZYPz[YQh[XNiZHXjdoVie2ViaX6gO{1FUENibHX2[Yx{KGG2IEGgeW0h[nliTFOtUXMwT0NvTWOgZY5idHm|aYO= NVnC[XFHRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[3PFk3PTdpPkK2O|g6PjV5PD;hQi=>
Neuro2a NUDwS4pqTnWwY4Tpc44h[XO|YYm= NG[5PXUyKHWP M1nsemlvcGmkaYTpc44hd2ZiRGKyOEBqdiCvb4Xz[UBP\XW{b{LhJINmdGy|IHHzd4V{e2WmIHHzJIRm[3KnYYPlJIlvKDdvRFjDJIxmfmWuczDheEAyKHWPIHL5JGxENU2VL1fDMW1UKGGwYXz5d4l{ NFO5T5k9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{Nke4PVY2Pyd-Mk[3PFk3PTd:L3G+
Neuro2a Mk\YSpVv[3Srb36gZZN{[Xl? MkXrNUB2VQ>? M{nqOmlvcGmkaYTpc44hd2ZiSF3HR49CKHKnZIXjeIF{\SCrbjDEbINzPy2mZX\pZ4lmdnRibX;1d4UhVmW3cn:yZUBk\WyuczDhd5Nme3OnZDDhd{Bl\WO{ZXHz[UBqdiB5LVTIR{Bt\X[nbIOgZZQhOSC3TTDifUBNSy2PUz;HR{1OWyCjbnHsfZNqew>? MUm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjd6OU[1O{c,OjZ5OEm2OVc9N2F-
MCF-7 MXfGeY5kfGmxbjDhd5NigQ>? NUDUcWVXOTBidV2= NUfzN2I2OjRiaILz NIT4ZVRCdnSjZ3;ubZN1KGGldHn2bZR6KGG2IF35Z{11[WepZXSgVnhT[WyyaHGgLJVvc26xd36gc5Jq\2mwKTDlfJBz\XO|ZXSgbY4hcHWvYX6gUWNHNTdiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kA6NWOrcz3SRUBqdmS3Y3XkJJJm[2WydH;yJJRz[W6|YXP0bZZifGmxbjDheEAyOCC3TTDh[pRmeiB{NDDodpMh[nlibIXjbYZmemG|ZTDy[ZBwenSncjDn[Y5mKGG|c3H5 M1;VflxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ6MEi5N|Q4Lz5{OEC4PVM1PzxxYU6=
MCF-7 NWjnNox[TnWwY4Tpc44h[XO|YYm= MoqwNUB2VQ>? MYGyOEBpenN? MYrBcpRi\2:waYP0JIFkfGm4aYT5JIF1KE27Yz30ZYdo\WRiUmjSZYxxcGFiKIXub45wf25ib4Lp[4lvMSCneIDy[ZN{\WRiaX6gbJVu[W5iTVPGMVch[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjC5MYNqey2UQTDpcoR2[2WmIILlZ4VxfG:{IITyZY5{[WO2aY\heIlwdiCjdDCxJJVOKGGodHXyJFI1KGi{czDifUBtfWOrZnXyZZNmKHKncH;yeIVzKGenbnWgZZN{[Xl? M1y4NFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ6MEi5N|Q4Lz5{OEC4PVM1PzxxYU6=

他の多くの細胞株試験データをご覧になる場合はこちらをクリックして下さい

アッセイ
Methods Test Index PMID
Western blot
Nrf2 / NQO1 / HO-1 ; 

PubMed: 28542559     


Western blot analysis of Nrf2, NQO1, and HO-1 in statin-treated VSMCs. Cells were exposed to fluvastatin and pitavastatin for 24 h at the indicated dosages.

Flt1 / Flk1 ; 

PubMed: 21301413     


Immunoblots showing Flt-1 and Flk-1 expression in HUVECs in the absence or presence of pitavastatin. Representative data of three independent experiments with similar results.

VEGF / p-Akt / AKT / Jagged-1 / c-Notch1 / Notch-1 / Hes-1 ; 

PubMed: 21301413     


Immunoblots showing the time course of pitavastatin (100 nmol/l)-induced Akt and Notch1 activation, VEGF, Notch1 ligand (Jagged-1) and Hes-1 expression in human umbilical vein endothelial cells (HUVECs). Activation of Akt was assessed by Ser473 phosphorylation of Akt (p-Akt) relative to the total Akt (t-Akt). Activation of Notch1 was determined by the amount of cleaved Notch1 (c-Notch1) relative to total Notch1 (t-Notch1). Representative blots of three independent experiments with similar results.

28542559 21301413
Growth inhibition assay
Cell number; 

PubMed: 21301413     


Cell counts (human umbilical vein endothelial cells) in the absence or presence of pitavastatin (10 nmol/l–1.0 μmol/l).  Effects of mevalonate (200 μmol/l), LY294002 (Ly)(10 μmol/l), Akt inhibitor SH-5 (10 μmol/l), NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (1 mmol/l) and γ-secretase inhibitor DAPT (20 μmol/l) on cell numbers were also determined. *P<0.007 compared with control and **P<0.001 compared with control and #P<0.001 compared with pitavastatin (100 nmol/l). n = 8 in each group.

21301413
体内試験 Pitavastatin decreases the tumor growth and improved the survival of tumor-bearing mice[5]. Pitavastatin exerts a protective effect on dilated cardiomyopathy possibly through down-regulating the circulating and local RAS, followed by inhibition of PKCb2 phosphorylation, and consequently promoting the phosphorylation of PLB as well as the activity and the expressions of SERCA2a and RyR2, whereby heart function is preserved in the development of DCM[6].

お薦めの試験操作(参考用のみ)

細胞試験:

[5]

- 合併
  • 細胞株: Huh-7 and SMMC7721
  • 濃度: 5 μM
  • 反応時間: 1, 2, 4, 6 days
  • 実験の流れ:

    The Huh-7 cells and SMMC7721 cells are split into 96-well dishes at 5,000 cells/well and treated with the indicated dosage of pitavastatin for 48 hours or 5 µM pitavastatin for 1, 2, 4, 6 days respectively. The cells are incubated with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and formed formazan in the liver cells. Formazan is dissolved in DMSO, and the absorbance is measured at the wavelength of 570 nm. The cells treated with DMSO are used as a control group. The relative cell number of each group is calculated as pitavastatin-treated group/cell number in the DMSO-treated group.


    (参考用のみ)
動物試験:

[6]

- 合併
  • 動物モデル: C57BL/6 mice
  • 投薬量: 1 or 3 mg/kg/d
  • 投与方法: oral
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 51 mg/mL (57.89 mM)
Water Insoluble
Ethanol Insoluble

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。

化学情報

分子量 880.98
化学式

C50H46CaF2N2O8

CAS No. 147526-32-7
Storage powder
in solvent
別名 P-872441, itavastatin, nisvastatin
Smiles C1CC1C2=NC3=CC=CC=C3C(=C2C=CC(CC(CC(=O)[O-])O)O)C4=CC=C(C=C4)F.C1CC1C2=NC3=CC=CC=C3C(=C2C=CC(CC(CC(=O)[O-])O)O)C4=CC=C(C=C4)F.[Ca+2]

投与溶媒組成計算器(クリア溶液)

ステップ1:実験データを入力してください。(実験操作によるロスを考慮し、動物数を1匹分多くして計算・調製することを推奨します)
投与量 mg/kg 動物平均体重 g 投与体積(動物毎) ul 動物数
ステップ2:投与溶媒の組成を入力してください。(ロット毎に適した溶解組成が異なる場合があります。詳細については弊社までお問い合わせください)
% DMSO % % Tween 80 % ddH2O
計算リセット

便利ツール

モル濃度計算器

モル濃度計算器

求めたい質量、体積または濃度を計算してください。

質量 (mg) = 濃度 (mM) x 体積 (mL) x 分子量 (g/mol)

モル濃度計算器方程式

  • 質量
    濃度
    体積
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備するために必要な希釈率を計算してください。Selleck希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 入力 出力 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

質量 濃度 体積 分子量

臨床試験

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04643093 Active not recruiting Drug: Pitavastatin|Drug: Ezetimibe|Drug: 1PC111 Primary Hypercholesterolemia|Mixed Dyslipidemias Orient Pharma Co. Ltd. August 1 2020 Phase 3
NCT03717064 Completed Drug: RO7049389|Drug: Pitavastatin Healthy Volunteers Hoffmann-La Roche November 7 2018 Phase 1
NCT02956590 Active not recruiting Drug: Pitavastatin|Drug: Placebo Dyslipidemia|Obesity HealthCore-NERI|National Heart Lung and Blood Institute (NHLBI) May 1 2018 Phase 3

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須

よくある質問(FAQ)

  • 質問1:

    How to prepare the solution of the compound (S1759) for in vivo use?

  • 回答:

    You could use the formulation: 5% DMSO +40%PEG 300+5%Tween80+ddH2O for i.p., at a working concentration of 12.5mg/ml, stable for no longer than 40min.

HMG-CoA Reductaseシグナル伝達経路

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID