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[DNA Damage/DNA Repair]

Temozolomide,85622-93-1,IC-0212432

Price : $37.50Price : ￥375.00

Temozolomide is an oral activity alkylating agent that induces the formation of O6-methylguanine in DNA, which mispairs with thymine during the following cycle of DNA replication, leading to activation of the apoptotic pathways, Temozolomide could crosses the blood-brain barrier and is indicated for malignant gliomas and metastatic melanomas [1]. Temozolomide induced cell cycle arrest at G2/M and to eventually lead to apoptosis [2]. At physiologic pH it is converted to the short-lived active compound, MTIC. MTIC is further hydrolyzed to 5-amino-imidazole-4-carboxamide (AIC) and to methylhydrazine. The cytotoxicity of Temozolomide is mediated by its addition of methyl groups at N7 and O6 sites on guanines and the O3 site on adenines in genomic DNA. Alkylation of the O6 site on guanine leads to the insertion of a thymine instead of a cytosine opposite the methylguanine during subsequent DNA replication, and this can result in cell death [3]. Lymphoma cell counts performed 72 hours after treatment showed that the IC50 of Temozolomide was 44 µM (35-58 µM) when used alone and 16 µM (12-26 µM) when combined with NU1025 [1]. A time-related response in DNA strand-break formati......
[DNA Damage/DNA Repair]

SCR7,1533426-72-0,IC-0212621

Price : $420.00Price : ￥4200.00

Scr7 is a DNA ligase IV inhibitor, initially identified as an anti-cancer agent [1]. Scr7 targets the DNA binding domain of DNA ligase IV, reducing its affinity for double strand breaks (DSBs) and inhibiting its function. Scr7 also inhibits DNA ligase III (but not DNA ligase I), albeit less efficiently. Cells were treated with doxycycline to induce Cas9 expression, with various concentrations of Scr7 for 24 h. Scr7 maintained cells capable of entering S/G2 phase, which is necessary for HDR. [1] Treatment of mice with Scr7 affects lymphocyte development, as DNA ligase IV plays a key role in the joining of coding ends during V(D)J recombination by means of C-NHEJ16. The defects in lymphocyte development upon Scr7 treatment are transient and reversible, due to the noncovalent mode of binding of Scr7. Scr7 enhanced the frequency of HDR by transiently blocking NHEJ (with the exception of DNA ligase I–dependent alt-NHEJ), resulting in precise genome editing by CRISPR-Cas9 in both cultured cells and in mice. [2]
[DNA Damage/DNA Repair]

Bleomycin Sulfate,9041-93-4,IC-0213377

Price : $122.00Price : ￥1220.00

Bleomycin is produced by Streptomyces verticillis. The Bleomycin molecule has two main structural components; a bithiazole component which partially intercalates into the DNA helix, parting the strands, as well as pyrimidine and imidazole structures, which bind iron and oxygen forming an activated complex capable of releasing damaging oxidants in close proximity to the polynucleotide chains of DNA. This may lead to chain scission or structural modifications leading to release of free bases or their propenal derivatives. It has potent tumor killing properties which have gained it an critical role in cancer chemotherapy. It causes little marrow suppression, but the major adverse is pulmonary toxicity effect.[1] In vitro, Bleomycin reacts with DNA which has previously been treated with a sulfhydryl compound, and cause a decrease in its melting temperature (Tm). In the reactions in vitro, strand scission in DNA has been confirmed which indicate that in the presence of a sulfhydryl compound in vitro, Bleomycin binds to DNA, and causes single-strand scission. The scission of DNA may be the cause of the inhibition of thymidine incorporation into DNA of growing cells and the i......
[DNA Damage/DNA Repair]

CX-5461,1138549-36-6,IC-0213566

Price : $66.00Price : ￥660.00

CX-5461 is a potent and orally bioavailable small-molecule inhibitor of rRNA synthesis that specifically inhibits RNA polymerase (Pol) I-driven transcription with IC50 value of 142 nM. CX-5461 exhibits antiproliferative activity against human pancreatic tumor cells MIA Paca-2, human melanoma cells A375 and colorectal carcinoma cells HCT-116 with EC50 values of 74, 58, and 167 nmol/L, respectively. [1]. CX-5461 was revealed to inhibit Pol I transcription via promoting the stabilization of p53. In addition, CX-5461 has been demonstrated to induce autophagy and senescence but not apoptosis in MIA Paca-2 and A375 cell lines. In vivo, CX-5461 has shown to suppress tumor volume in both MIA Paca-2 and A375 derived xenograft mice models [1].
[DNA Damage/DNA Repair]

Gemcitabine,95058-81-4,IC-0213755

Price : $108.00Price : ￥1080.00

Gemcitabine is an inhibitor of DNA synthesis [1]. DNA synthesis is a natural creation of deoxyribonucleic acid (DNA) molecules and plays an important role in cell growth. Gemcitabine is an active chemotherapeutic agents that disrupt DNA replication. In tumor cells, gemcitabine activated checkpoint kinase 2 (Chk2) and ataxia-telangiectasia mutated kinase (ATM), which regulated apoptosis, DNA repair and cell-cycle arrest. Also, gemcitabine activated the Rad9-Hus1-Rad1 complex and the protein kinases ATM and ATR and checkpoint kinase 1 (Chk1), which blocked cell-cycle progression and influence DNA repair [1]. Gemcitabine is a DNA synthesis inhibitor with anti-tumor activity. In human osteosarcoma cell lines HOS and MG63, gemcitabine inhibited DNA synthesis and induced apoptosis [2]. In C3H mice inoculated with murine osteosarcoma cell line LM8, gemcitabine induced cell apoptotics and reduced the size of primary tumor. Also, it inhibited metastatic lesions in the lung [2]. In C57Bl/6 mice infected with LP-BM5 murine leukemia virus, gemcitabine significantly inhibited disease progression. Also, gemcitabine reduced spleen size, provirus levels and plasma IgM [3].
[DNA Damage/DNA Repair]

Oxaliplatin,61825-94-3,IC-0213944

Price : $67.50Price : ￥675.00

Oxaliplatin is a cytotoxic chemotherapy drug used to treat cancer. Oxaliplatin works by interfering with the development of DNA in a cell. This helps to treat cancer which is caused by cells rapidly growing and dividing out of control. Oxaliplatin can induce DNA damage in cancer cells. Besides,oxaliplatin can interfere with the cell cycle, promote apoptosis, and induce autophagy in tumor cells[2,3]. Oxaliplatin inhibited cell viability, migration, and cloning formation of OSCC cells and induced cell death in vitro[1]. Oxaliplatin inhibited the growth of HCCLM3 and Hep3B cells.Downregulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL and upregulation of the pro-apoptotic protein Bax during oxaliplatin-induced apoptosis[6]. Oxaliplatin was found to be active against C32 and G361 cell lines with IC50 values of 49.48 and 9.07 uM (1 h exposure), 9.47 and 1.30 uM (4 h exposure), and 0.98 and 0.14 uM (24 h exposure), respectively. At a 24 h exposure oxaliplatin appears to be significantly more active than cisplatin against the G361 cell line[4]. 85-88% of all platinum from oxaliplatin was bound to plasma proteins within the first 5 h with an average half-life of 1.71 +/-......

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