製品コードS8039 別名:NSC 750424



PU-H71 is a potent and selective inhibitor of HSP90 with IC50 of 51 nM. Phase 1.

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JPY 16102.00
JPY 36520.00


  • Effects of low-level HSP90 inhibition (by ganetespib, 2-5 nM; PU-H71, 40-70 nM) or febrile-range temperature (39 ℃) on HSP70 and HSP90 protein levels in FANCA wild-type cells. High-level HSP90 inhibition (ganetespib, 25 nM; PU-H71, 300 nM) as well as proteotoxic proteasomal inhibition (MG132, 2.5 mM) induced the expression of HSP70. Constitutive (upper band: C) and inducible forms (lower band: I) of HSP70 are indicated. HSP90 levels are shown for comparison.

    Cell, 2017, 168(5):856-866. PU-H71 purchased from Selleck.


HSP (e.g. HSP90)阻害剤の選択性比較


製品説明 PU-H71 is a potent and selective inhibitor of HSP90 with IC50 of 51 nM. Phase 1.
特性 Purine-based, HSP90-selective inhibitor.
HSP90 [1]
51 nM

PU-H71 (1 μM) potently suppresses the growth of triple-negative breast cancers (TNBC) cell lines MDA-MB-468, MDA-MB-231, and HCC-1806 with IC50 of 65, 140 and 87 nM, respectively. PU-H71 (1 μM) kills 80%, 65%, and 80% of the initial population of MDA-MB-468, MDA-MB-231, and HCC-1806 cells, respectively. PU-H71 (0.25-1 μM) induces a dose-dependent degradation or inactivation of tumor driving molecules, including EGFR, IGF1R, HER3, c-Kit, Raf-1and Akt. Treatment for 24 h with 1 μM PU-H71, augments the percent of cells in G2-M phase of MDA-MB-468 to 69%, mediated by reduction in CDK1 and Chk1 expression. PU-H71 induces apoptosis in TNBC in part by inactivation and downregulation of Akt and Bcl-xL. PU-H71 leads to a proteasome-mediated reduction in IRAK-1 and TBK1 levels, resulting in approximately 84% and 90% reduction in NF-κB activity in MDA-MB-231 cells treated with 0.5 and 1μM PU-H71, respectively. PU-H71 markedly contains MDA-MB-231 cell invasion, with 90% suppression at 1 μM. [1] PU-H71 (2.5 μM) generates endoplasmic reticulum (ER) stress and activated the Unfolded Protein Response (UPR) as evidenced by XBP1 mRNA splicing (2.3-fold) and up-regulation of Grp94 (3.7-fold), Grp78 (4.9-fold), and CHOP (48-fold) protein expression and ATF4 (1.8-fold) mRNA expression. PU-H71 (1 μM) induces the mitochondrial pathway of apoptosis in HeLa cells, mediated by caspase but not calpain activation. In response to PU-H71-induced ER stress, apoptosis is triggered in melanoma, cervix, colon, liver and lung cancer cells, but not in normal human fibroblasts. PU-H71 is able to induce apoptosis overcoming the resistance conferred by Bcl-2. [2] PU-H71 (30 n M) significantly reduces NOS2 activity (60% reduction) and expression in LI (1 μg/mL LPS and 5 ng/mL IFN γ)-stimulated astrocytes via inhibiting NF-κB element activation. PU-H71 displays similar effects on microglial cells as on astrocytes, with 50 nM PU-H71 needed to significantly reduce the LPS dependent nitrite release. [3]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MDA-MB-468 cells MWLGeY5kfGmxbjDhd5NigQ>? MmLmTY5pcWKrdH;yfUBi[3Srdnn0fUBi\2GrboP0JGh{eDlyIHnuJIh2dWGwIHLy[YF{fCClYX7j[ZIhVUSDLV3CMVQ3QCClZXzsJIxqdmVuIFXDOVA:OC5yMUCyJO69VQ>? NITDPFMyPjN7MkiyNy=>
SKBr3 cells M4Xqb2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7 M{H0eGdzd3e2aDDpcohq[mm2aX;uJIlvKGi3bXHuJIJz\WG|dDDjZY5k\XJiU1vCdlMh[2WubDDsbY5mKHW|aX7nJHNTSixiSVO1NF0xNjB3IN88US=> NHrHR2syPjN7MkiyNy=>
MCF7 cells NELSW2JHfW6ldHnvckBie3OjeR?= M1qwR|I1KGh? M2[3d2lvcGmkaYTpc44hd2ZiSIPwPVAhcW5iaIXtZY4hVUOINzDj[YxteyCjc4Pld5Nm\CCjczDI[ZIzKGyndnXsJIFnfGW{IEK0JIhzeyCkeTDX[ZN1\XKwIHLsc5QtKEmFNUC9NE4xPiEQvF2= MlnqNVg2PzF7Mkm=
MRC5 cells NI\EN|JEgXSxdH;4bYNqfHliYYPzZZk> NWnYcHlxS3m2b4TvfIlkcXS7IHHnZYlve3Ribn;ycYFtKGy3bneg[oljem:kbHHzeEBOWkN3IHPlcIwhdGmwZTygTWM2OD1zIN88US=> M4\ZOFE3Ozl{OEKz
NCI-H1299 cells M2\3N2Z2dmO2aX;uJIF{e2G7 MV:xNkBp M4XxSHJm\HWldHnvckBqdiCxeInn[Y4h[2:wc4XtdJRqd25icnH0[UBqdiCqdX3hckBPS0lvSEGyPVkh[2WubIOgbY5kfWKjdHXkJIZweiBzMjDodpM> NI\yO2UzPTN6M{mxOS=>
NCI-H69 cells MXnGeY5kfGmxbjDhd5NigQ>? NUXsT5gxOjRiaB?= NUfyN5N7SmmwZHnu[{Bi\m[rbnn0fUB1dyCKU2C5NEBqdiCqdX3hckBPS0lvSE[5JINmdGy|IHHmeIVzKDJ2IHjyd{BjgSCobIXvdoV{[2WwY3WgdI9t[XKrenH0bY9vKGG|c3H5 MkS1NVc3ODN3NEC=
NCI-H187 cells NYH2V3ZtTnWwY4Tpc44h[XO|YYm= MUKyOEBp NGO4TlRDcW6maX7nJIFn\mmwaYT5JJRwKEiVUEmwJIlvKGi3bXHuJG5EUS2KMUi3JINmdGy|IHHmeIVzKDJ2IHjyd{BjgSCobIXvdoV{[2WwY3WgdI9t[XKrenH0bY9vKGG|c3H5 NU\QNlkxOTd4MEO1OFA>
NCI-H510 cells Mof3SpVv[3Srb36gZZN{[Xl? MnjyNlQhcA>? NF\nPZhDcW6maX7nJIFn\mmwaYT5JJRwKEiVUEmwJIlvKGi3bXHuJG5EUS2KNUGwJINmdGy|IHHmeIVzKDJ2IHjyd{BjgSCobIXvdoV{[2WwY3WgdI9t[XKrenH0bY9vKGG|c3H5 NEXROm0yPzZyM{W0NC=>
SKBR3 cells MmH5SpVv[3Srb36gZZN{[Xl? NVmzWI1pOjRiaB?= MmjCRolv\GmwZzDh[oZqdmm2eTD0c{BJW1B7MDDpckBpfW2jbjDTT2JTOyClZXzsd{Bi\nSncjCyOEBpenNiYomg[ox2d3Knc3PlcoNmKHCxbHHybZpifGmxbjDhd5NigQ>? NHLWWZgyPzZyM{W0NC=>
NCI-H526 cells Ml;5SpVv[3Srb36gZZN{[Xl? M1;4V|Eh|ryP MkHENlQhcA>? MmTiRolv\GmwZzDh[oZqdmm2eTD0c{BJW1B7MDDpckBpfW2jbjDOR2kuUDV{NjDj[YxteyCjdDCxJJVOKGGodHXyJFI1KGi{czDifUBndHWxcnXzZ4Vv[2VicH;sZZJqgmG2aX;uJIF{e2G7 MYWxO|YxOzV2MB?=
H69AR cells MmXySpVv[3Srb36gZZN{[Xl? MoDsPVYhcA>? NIHzb5dKdmirYnn0bY9vKG:oIFjTVFkxNW2nZHnheIVlKGGwdHnhdI9xfG:2aXOgZYN1cX[rdImgbY4hcHWvYX6gTFY6SVJiY3XscJMh[XO|ZYPz[YQh[XNiaX7keYN1cW:wIH;mJINmdGxiZ4Lve5RpKGG{cnXzeEBifCBzMDDh[pRmeiB7NjDodpMh[nlicILvdIllcXWvIHnv[Ill\SC|dHHpcolv\y2kYYPl[EBndG:5IHP5eI9u\XS{eR?= MXexO|YxOzV2MB?=
NCI-H526 cells MXfGeY5kfGmxbjDhd5NigQ>? NHPSRWozPCCq NVXtR2hySmmwZHnu[{Bi\m[rbnn0fUB1dyCKU2C5NEBqdiCqdX3hckBPS0lvSEWyOkBk\WyuczDh[pRmeiB{NDDodpMh[nliZnz1c5Jme2OnbnPlJJBwdGG{aYrheIlwdiCjc4PhfS=> MoTsNVc3ODN3NEC=


体内試験 PU-H71 administered at 75 mg/kg a.d. in the MDA-MB-231 model, induces a 100% complete response, and tumors are reduced to scar tissue after 37 days of treatment, accompanied with reduction in many proliferative and anti-apoptotic molecules, namely an 80%, 95%, 99%, 80%, and 65% decrease in EGFR, HER3, Raf-1, Akt, and p-Akt, respectively. PU-H71 (75 mg/kg, 3 times per week) induces a 96% inhibition of tumor growth, accompanied by an 60% reduction in tumor cell proliferation, an 85% decline in activated Akt associated with survival and high invasive potential, and a 6-fold increase in apoptosis. [1]




+ 展開

HSP90 binding assay:

Measurements are performed in black 96-well microtiter plates. Cell lysates are prepared by rupturing cellular membranes by freezing at -70℃ and dissolving the cellular extract in HFB [20 mM Hepes (K), pH 7.3, 50 mM KCl, 5 mM MgCl2, 20 mM Na2MoO4, 0.01% Nonidet P-40] with added protease and phosphatase inhibitors. Saturation curves are recorded in which fluorescently labeled geldanamycin (Cy3B-GM) (3 nM) is treated with increasing amounts of cellular lysates. The amount of lysate that results in polarization (mP) readings corresponding to 90%-99% bound ligand is chosen for the competition study. Here, each 96-well plate contains 3 nM Cy3B-GM, cellular lysate (amounts as determined and normalized to total Hsp90 as determined by Western blot analysis using Hsp90 purified from HeLa cells as standard) and tested Hsp90 inhibitor in a final volume of 100 μL. The plate is left for 24 h on a shaker at 4 ℃, and the fluorescence polarization (FP) values in mP are recorded. EC50 values are determined as the competitor concentrations at which 50% of the Cy3B-GM is displaced. FP measurements are performed on an Analyst GT microplate reader.


+ 展開
  • 細胞株: Human triple-negative breast cancers cell line MDA-MB-231
  • 濃度: ~5μM
  • 反応時間: 3 days
  • 実験の流れ:

    Exponentially growing MDA-MB-231 cells are seeded into black 96-well microtiter plates and incubated in medium containing either vehicle control (DMSO) or compounds for the indicated time at 37 ℃. Plates containing 3 replicate wells per assay condition are seeded at a density of 8×103 cells for each cell line in 100μL medium. After exposure of cells to the Hsp90 inhibitors, plates are equilibrated to room temperature (20-25 ℃) for approximately 30 min, and 100 μL CellTiter-Glo reagent are added to each well. Plates are mixed for 2 min on an orbital shaker and then incubated for 15 min to 2 h at room temperature. The luminescence signal in each well is measured in an Analyst GT microplate reader.



+ 展開
  • 動物モデル: Human triple-negative breast cancers xenografts MDA-MB-231
  • 製剤: PBS
  • 投薬量: 75 mg/kg
  • 投与方法: i.p. on an alternate day schedule

溶解度 (25°C)

体外 DMSO 100 mg/mL (195.17 mM)
Ethanol 100 mg/mL (195.17 mM)
Water 34 mg/mL warmed (66.35 mM)

* 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。


分子量 512.37

C18 H21 I N6 O2 S

CAS No. 873436-91-0
in solvent
別名 NSC 750424





質量 (g) = 濃度 (mol/L) x 体積 (L) x 分子量 (g/mol)


  • 質量





開始濃度 x 開始体積 = 最終濃度 x 最終体積


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

  • C1



  • 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):




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


質量 濃度 体積 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03373877 Recruiting Myelofibrosis|Primary Myelofibrosis|Post-polycythemia Vera Myelofibrosis|Post-essential Thrombocythemia Myelofibrosis Samus Therapeutics Inc. May 24 2018 Phase 1
NCT03166085 Recruiting Metastatic Breast Cancer Memorial Sloan Kettering Cancer Center|Samus Therapeutics Inc. May 23 2017 Phase 1
NCT01393509 Active not recruiting Metastatic Solid Tumor|Lymphoma|Myeloproliferative Neoplasms (MPN) Memorial Sloan Kettering Cancer Center July 2011 Phase 1
NCT01581541 Terminated Solid Tumors|Lymphoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) April 26 2011 Phase 1
NCT01269593 Recruiting Non-Hodgkin''s Lymphoma|Myeloma|Active Solid Malignancy Memorial Sloan Kettering Cancer Center|Samus Therapeutics December 2010 Early Phase 1



Handling Instructions


  • * 必須

HSP (e.g. HSP90)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