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  • (a) H23 cells exposed for 0–24 h to TW-37 (10 uM) with and without ZVAD.fmk (50 uM) were monitored for apoptotic morphology using electron microscopy (scale bar, 5 mm). % PS positive cells indicate the percentage of apoptotic cells, characterised by PS externalisation.

    Cell Death Differ 2013 20, 1475-84. TW-37 purchased from Selleck.

    (b) Whole-cell lysates of H23 cells exposed for 0–24 h to TW-37 (10 uM) were probed with antibodies against PARP and caspase-9. The appearance of both the p89 processed form of PARP and the p35 form of caspase-9 were characteristic of the intrinsic pathway of apoptosis.

    Cell Death Differ 2013 20, 1475-84. TW-37 purchased from Selleck.

  • (c) Whole-cell lysates of BAK-reconstituted and -deficient Jurkat cells exposed for 0–24 h to TW-37 (10 uM ) were probed as in B. % PS positive cells indicate the percentage of apoptotic cells, characterised by PS externalisation.

    Cell Death Differ 2013 20, 1475-84. TW-37 purchased from Selleck.

    (d) Electron micrographs of control and TW-37 (10 uM for 24 h); treated BAK-reconstituted and -deficient Jurkat cells reveal a dependence on BAK for TW-37- mediated apoptosis (scale bar, 5 um)

    Cell Death Differ 2013 20, 1475-84. TW-37 purchased from Selleck.

  • MCL-1 is a key anti-apoptotic BCL-2 family member that regulates ER membrane reorganisation. (a) Pan-BCL-2 family inhibitors induce ER membrane reorganisation more potently than BCL-2 and BCL-XL-specific inhibitors. Apogossypol (10 μM) and TW37 (20 μM) induced extensive membrane reorganisation, assessed by BAP31 staining in HeLa cells, within 4 h of exposure, whereas ABT-737 (20 μM) induced modest reorganisation after 8 h and the inactive enantiomer ABT-737E (20 μM) failed to induce reorganisation (scale bar, 20 μm).

    Cell Death Differ 2012 19, 1896-907. TW-37 purchased from Selleck.

    MEF cells were treated for  24 hours with the Bcl-2 antagonists  TW-37at the indicated doses.Acute survival was monitored by propidium iodide uptake assays(red lines).Long term survival(red line) was measured by replacing the drug-containing media with normal media and incubating the cells until visible colonies formed.Clonogenic survival is expressed relative to the numbers of colonies formed following 24 hours incubation in normal media(lacking drugs).

    Dr. Christine Hawkins of La Trobe University. TW-37 purchased from Selleck.

  • MDB-MA-231 cells were exposed to 30 um cisplatin in the absence or in thepresence of 100 nm TW-37.The cell were stained with Hoechst 33342,MitoTracker Red and Yo-pro-1.



    Dr. Zhang of Tianjin Medical University. TW-37 purchased from Selleck.




製品説明 TW-37は一種の新たな非ペプチド類阻害剤で、無細胞試験で、組替えのBcl-2、Bcl-xLとMcl-1に作用する時のKi値が0.29μM、1.11μMと0.26μMにそれぞれ分かれることです。
Mcl-1 [1]
(Cell-free assay)
Bcl-2 [1]
(Cell-free assay)
Bcl-xL [1]
(Cell-free assay)
0.26 μM(Ki) 0.29 μM(Ki) 1.11 μM(Ki)

TW-37 targets the BH3-binding groove in Bcl-2 where proapoptotic Bcl-2 proteins bind, and shows higher affinity and selectivity for Bcl-2 and Mcl-1 over Bcl-xL with Ki values of 0.29 μM, 0.26 μM and 1.11 μM, respectively. [1] In vitro, TW-37 shows significant anti-proliferative and pro-apoptotic effect in a de novo chemo-resistant WSU-DLCL2 lymphoma cell line and primary cells obtained from a lymphoma patient without effects on normal peripheral blood lymphocytes. [1] TW-37 exhibits the inhibitory effect on both cell growth and cell death in endothelial cell with IC50 of approximately 1.8 μM without effect on the fibroblasts exposed to the same concentration range as the endothelial cells. In addition, TW37 also shows the anti-proliferation effects in MCF-7, LNCaP, and SLK tumor cell lines with the same or lower concentration range than those required to inhibit endothelial cell growth. [2]

体内試験 TW-37 shows a maximum tolerated dose (MTD) of 40 mg/kg for three i.v. injections in severe combined immunodeficient (SCID) mice when given alone, and enhances tumor inhibitory effect of cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP) regimen. [1] TW-37, administrated by i.v. produces the antiangiogenic effect by decreasing the density of functional human microvessels in the severe combined immunodeficient mouse model of human angiogenesis. [2] The combination of TW-37 and MEK inhibitors synergistically block melanoma cell growth in mice by a significant reduction in tumor volume and tumor mass. [3]


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Fluorescence polarization-based binding assay for recombinant Bcl-2, Bcl-XL, and Mcl-1 protein :

For this assay, the 21-residue BH3 peptide QEDIIRNIARHLAQVGDSMDR derived from Bid labeled with 6-carboxyfluorescein succinimidyl ester (FAM-Bid) and recombinant proteins derived from human Bcl-2,Bcl-X L,and Mcl-1 are employed. It is determined that FAM-Bid has a Ki of 11 nM to Bcl-2 protein,25 nM to Bcl-XL protein,and 5.7 nM to Mcl-1 protein. The competitive binding assay for Bcl-XL is same as that for Bcl-2 with the following exceptions: 30 nM Bcl-XL protein and 2.5 nM FAM-Bid peptide in the following assay buffer [50 mM Tris-Bis (pH 7.4) and 0.01% bovine gamma-globulin].
細胞試験: [2]
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  • 細胞株: HDMECs
  • 濃度: 0 - 100 μM
  • 反応時間: 96 hours
  • 実験の流れ: The sulforhodamine B (SRB) cytotoxicity assay is used as described. Briefly, optimal cell density for cytotoxicity assay is determined by growth curve analysis. HDMECs are seeded in a 96-well plate and allowed to adhere overnight. Drug or control is diluted in EGM2-MV and layered onto cells, which are allowed to incubate for times as indicated in the figures. Alternatively, HDMECs are coincubated with TW37 and 0 to 100 ng/mL recombinant human VEGF (rhVEGF)165 or 0 to 100 ng/mL recombinant human CXCL8. Cells are fixed on the plates by addition of cold trichloroacetic acid (10% final concentration) and incubation for 1 hour at 4 °C. Cellular protein is stained by addition of 0.4% SRB in 1% acetic acid and incubation at room temperature for 30 minutes. Unbound SRB is removed by washing with 1% acetic acid and the plates are air dried. Bound SRB is resolubilized in 10 mM unbuffered Tris-base and absorbance is determined on a microplate reader at 560 nm. Test results are normalized against initial plating density and drug-free controls. Data are obtained from triplicate wells per condition and are representative of at least three independent experiments
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  • 動物モデル: Athymic NCr-nu/nu mice bearing SK-Mel-147 melanoma xenografts
  • 製剤: TW-37 is resuspended in 1:1 Tween 80/ethanol (diluted 10-fold in 0.9% saline before use).
  • 投薬量: ~40 mg/kg
  • 投与方法: Administered via i.v. or i.p.

溶解度 (25°C)

体外 DMSO 115 mg/mL (200.45 mM)
Ethanol 4 mg/mL (6.97 mM)
Water slightly soluble or insoluble
体内 順序で溶剤を入れること:
30% propylene glycol, 5% Tween 80, 65% D5W
30 mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。


分子量 573.7


CAS No. 877877-35-5
in solvent
別名 N/A





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、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


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

  • 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


マス 濃度 ボリューム 分子量



Handling Instructions


  • * 必須


Bcl-2 Inhibitors with Unique Features


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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