1. Epigenetics
  2. DNA Methyltransferase
  3. Guadecitabine

Guadecitabine (Synonyms: SGI-110)

目录号: HY-13542 纯度: 98.00%

Guadecitabine (SGI-110) 是第二代 DNA 甲基转移酶 (DNMT) 抑制剂,可用于急性髓细胞性白血病 (AML) 和骨髓增生异常综合症 (MDS) 的研究。

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Guadecitabine Chemical Structure

Guadecitabine Chemical Structure

CAS No. : 929901-49-5

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Guadecitabine 的其他形式现货产品:

Customer Review

Other Forms of Guadecitabine:

Top Publications Citing Use of Products

    Guadecitabine purchased from MCE. Usage Cited in: Neoplasia. 2020 May 25;22(7):274-282.

    Immunoblot of the total RH30 and RH41 cell extracts treated with the indicated concentrations of SGI-110 or DMSO (control) for 5 days, probed with antibodies against FGFR4, FOXO1, IGF-1R and MYOD1.

    Guadecitabine purchased from MCE. Usage Cited in: Neoplasia. 2020 May 25;22(7):274-282.

    Immunofluorescent analysis of RH30 and RH41 cells treated with DMSO or indicated concentrations of SGI-110 for 5 days.

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    • 生物活性

    • 实验参考方法

    • 纯度 & 产品资料

    • 参考文献


    Guadecitabine (SGI-110) is a second-generation DNA methyltransferases (DNMT) inhibitor for research of acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS)[1].

    IC50 & Target[1]

    DNA Methyltransferase


    In Vitro

    Exposure to Guadecitabine induces the expression of investigated cancer/testis antigens (CTA) in CTA-negative cancer cells. Results show that Guadecitabine induces and/or strongly up-regulates the constitutive levels of MAGE-A3- and NY-ESO-1-specific mRNA expression in neoplastic cells of all histotypes investigated. Exposure to Guadecitabine significantly (p<0.05) up-regulates the constitutive levels of expression of HLA class I antigens, HLA-A2 allospecificity, and of the co-stimulatory molecule ICAM-1, on Mel 275 melanoma cells. Results show that treatment with Guadecitabine induces a significant (p<0.01) reduction in the constitutive methylation levels of CTA promoters in investigated cancer cells. Mean values of the percentage of demethylation induced by Guadecitabine in MAGE-A1 and NY-ESO-1 promoters are 57 and 30 %, in Mel 195, and 22 and 33 % in MZ-1257 RCC cells, respectively[2].

    In Vivo

    Guadecitabine (S110) is effective at retarding tumor growth. While the tumors do not shrink in size with Guadecitabine treatment, they experience very minimal growth while the tumors treated with PBS only show substantial growth. In addition, Guadecitabine induces much less toxicity as determined by mouse weight changes when given subcutaneously (SQ) compare to that with IP injections[3].

    Clinical Trial
    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years


    Solvent & Solubility
    In Vitro: 


    Cell Assay

    Cells (3 to 4×105) are seeded in a T75 tissue culture flask and treated 24 h later with Guadecitabine , by replacing the medium with fresh one containing 1 μM or 10 μM of Guadecitabine, every 12 h for 2 days (4 pulses) and then with fresh medium without drugs for additional 2 days. Control cultures are treated under similar experimental conditions in the absence of drug[2].

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

    Animal Administration

    Athymic nu/nu mice are inoculated subcutaneously (SQ) in the right hind flank with 107 EJ6 bladder cancer cells. After tumors reach 0.5 cm in diameter, animals are stratified into three groups with eight animals per group to begin treatments. Doses and dosing schedules are designed so that each group receives molar equivalents of Guadecitabine (S110). The agent is administered SQ once weekly at a dose of 12.2 mg/kg for Guadecitabine for three weeks. The study includes an appropriate PBS control group. Tumor sizes by caliper and body weight measurements are taken twice weekly to monitor tumor growth inhibition and tolerability[3].

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


    Purity: 98.00%

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    GuadecitabineSGI-110SGI110SGI 110DNA MethyltransferaseDNMTsDNA MTasesInhibitorinhibitorinhibit


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