标签归档：ctce

CTCE-9908

发表于由

CTCE-9908; 纯度: 99.69%

CTCE-9908 是一种有效的，选择性的 CXCR4 抑制剂。CTCE-9908 在表达 CXCR4 的卵巢癌细胞中诱导有丝分裂突变，诱导细胞毒性，抑制迁移。

CTCE-9908amp;;

CTCE-9908 Chemical Structure

CAS No. : 1030384-98-5

规格 价格 是否有货 数量
1 mg ￥2800 In-stock
5 mg ￥6900 In-stock
10 mg ; 询价 ;
50 mg ; 询价 ;

* Please select Quantity before adding items.

CTCE-9908 相关产品

bull;相关化合物库:

  • Bioactive Compound Library Plus
  • Peptide Library

生物活性

CTCE-9908 is a potent and selective CXCR4 antagonist. CTCE-9908 induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells[1][2].

IC50 Target[1]

CXCR4

;

体外研究
(In Vitro)

CTCE-9908 (0-300 μg/mL; for 10 d) inhibits migration and growth in CXCR4-expressing in ovarian cancer cell lines (IGROV, TOV21G and SKOV3). CTCE-9908 inhibits ovarian cancer cell migration to CXCL12. CTCE-9908 does not cause apoptosis or cellular senescence, but induces multinucleation, G2-M arrest, and abnormal mitosis in ovarian cancer cells. CTCE-9908 deregulates DNA damage checkpoint proteins and spindle assembly checkpoint proteins at G2-M phases of the cell cycle[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

CTCE-9908 (25, 50 and 100 mg/kg; s.c.; 5 days per week for 4.5 weeks) alone slows the rate of primary breast tumor growth, with a 45% inhibition of primary tumor growth at 3.5 weeks of treatment with 50 mg/kg in FVB/N TgN (MMTV-PyMT)634 male mice[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

1927.25

Formula

C86H147N27O23
CAS 号

1030384-98-5
Sequence Shortening

Sequence 1:KGVSLSYRK-NH2;Sequence 1′:KGVSLSYR (Amide bridge:Lys9-Arg8rsquo;)
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Stored under nitrogen

Powder -80deg;C 2 years
-20deg;C 1 year

*In solvent : -80deg;C, 6 months; -20deg;C, 1 month (stored under nitrogen)
溶解性数据
In Vitro:;

H2O : 33.33 mg/mL (17.29 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 0.5189 mL 2.5944 mL 5.1887 mL
5 mM 0.1038 mL 0.5189 mL 1.0377 mL
10 mM 0.0519 mL 0.2594 mL 0.5189 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (stored under nitrogen)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
参考文献

  • [1]. Joseph Kwong, et al. An antagonist of the chemokine receptor CXCR4 induces mitotic catastrophe in ovarian cancer cells. Mol Cancer Ther. 2009 Jul;8(7):1893-905.

    [2]. Saima Hassan, et al. CXCR4 peptide antagonist inhibits primary breast tumor growth, metastasis and enhances the efficacy of anti-VEGF treatment or docetaxel in a transgenic mouse model. Int J Cancer. 2011 Jul 1;129(1):225-32.

CTCE-9908 TFA

发表于由

CTCE-9908 TFA;

CTCE-9908 TFA 是一种有效的，选择性的 CXCR4 抑制剂。CTCE-9908 TFA 在表达 CXCR4 的卵巢癌细胞中诱导有丝分裂突变，诱导细胞毒性，抑制迁移。

CTCE-9908 TFAamp;;

CTCE-9908 TFA Chemical Structure

规格 是否有货
100 mg ; 询价 ;
250 mg ; 询价 ;
500 mg ; 询价 ;

* Please select Quantity before adding items.

CTCE-9908 TFA 的其他形式现货产品:

CTCE-9908

生物活性

CTCE-9908 TFA is a potent and selective CXCR4 antagonist. CTCE-9908 TFA induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells[1][2].

IC50 Target[1]

CXCR4

;

体外研究
(In Vitro)

CTCE-9908 TFA (0-300 μg/mL; for 10 d) inhibits migration and growth in CXCR4-expressing in ovarian cancer cell lines (IGROV, TOV21G and SKOV3). CTCE-9908 TFA inhibits ovarian cancer cell migration to CXCL12. CTCE-9908 TFA does not cause apoptosis or cellular senescence, but induces multinucleation, G2-M arrest, and abnormal mitosis in ovarian cancer cells. CTCE-9908 TFA deregulates DNA damage checkpoint proteins and spindle assembly checkpoint proteins at G2-M phases of the cell cycle[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

CTCE-9908 TFA (25, 50 and 100 mg/kg; s.c.; 5 days per week for 4.5 weeks) alone slows the rate of primary breast tumor growth, with a 45% inhibition of primary tumor growth at 3.5 weeks of treatment with 50 mg/kg in FVB/N TgN (MMTV-PyMT)634 male mice[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

2041.27

Formula

C88H148F3N27O25
Sequence Shortening

Sequence 1:KGVSLSYRK-NH2;Sequence 1′:KGVSLSYR (Amide bridge:Lys9-Arg8rsquo;)
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent Solubility
In Vitro:;

H2O

Peptide Solubility and Storage Guidelines:

1.;;Calculate the length of the peptide.

2.;;Calculate the overall charge of the entire peptide according to the following table:

; Contents Assign value
Acidic amino acid Asp (D), Glu (E), and the C-terminal -COOH. -1
Basic amino acid Arg (R), Lys (K), His (H), and the N-terminal -NH2 +1
Neutral amino acid Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q) 0

3.;;Recommended solution:

Overall charge of peptide Details
Negative (lt;0) 1.;;Try to dissolve the peptide in water first.
2.;;If water fails, add NH4OH (lt;50 μL).
3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0) 1.;;Try to dissolve the peptide in water first.
2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution.
3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0) 1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first.
2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献

  • [1]. Joseph Kwong, et al. An antagonist of the chemokine receptor CXCR4 induces mitotic catastrophe in ovarian cancer cells. Mol Cancer Ther. 2009 Jul;8(7):1893-905.

    [2]. Saima Hassan, et al. CXCR4 peptide antagonist inhibits primary breast tumor growth, metastasis and enhances the efficacy of anti-VEGF treatment or docetaxel in a transgenic mouse model. Int J Cancer. 2011 Jul 1;129(1):225-32.