Mitomycin C |
Catalog No.: GC12353 |
Mitomycin C, a kind of antibiotic isolated from Streptomyces caespitosus or Streptomyces lavendulae, inhibits DNA synthesis through covalent mitomycin C-DNA adduct with EC50 values of 0.14μM in PC3 cells.
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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Purity: >98.00%
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- Datasheet
Cell experiment [1]: | |
Cell lines |
HCT116, HT-29 |
Preparation Method |
Ten millimolar Mitomycin C is prepared in 100% dimethyl sulfoxide, stored as small aliquots at -80°C and then diluted as needed in cell culture medium. |
Reaction Conditions |
5 μM,12 or 24h |
Applications |
Mitomycin C is a mitomycin that is used as a chemotherapeutic agent by virtue of its antitumour activity. Mitomycin C not only potentiates TRAIL-induced apoptosis in HCT116 (p53−/−) colon cancer cells but also sensitizes TRAIL- resistant colon cancer cells HT-29 to the cytokine. Mitomycin C inhibits HT-29 with IC50 of 40 nM. |
Animal experiment [2]: | |
Animal models |
Nude mice (6 weeks) injected subcutaneously with 1 × 106 HCT116 (p53−/−) or 2 × 106 HT-29 cells mixed with Matrigel |
Preparation Method |
Ten millimolar Mitomycin C is prepared in 100% dimethyl sulfoxide, stored as small aliquots at -80°C and then diluted as needed in cell culture medium. |
Dosage form |
1 mg/kg, Intraperitoneal injection |
Applications |
Mitomycin C suppresses tumor growth significantly and does not impact the weight of the mice with TRAIL, indicating that the therapeutic combination of Mitomycin C and TRAIL is well-tolerated and has anti-tumor activity in vivo. |
References: [1]. Cheng H, et al. Mitomycin C potentiates TRAIL-induced apoptosis through p53-independent upregulation of death receptors: evidence for the role of c-Jun N-terminal kinase activation. Cell Cycle. 2012 Sep 1;11(17):3312-23. [2]. Hodgkinson TJ, et al. Chemical synthesis and cytotoxicity of some azinomycin analogues devoid of the 1-azabicyclo[3.1.0]hexane subunit. Bioorg Med Chem Lett. 2000 Feb 7;10(3):239-41. |
Mitomycin C, a kind of antibiotic isolated from Streptomyces caespitosus or Streptomyces lavendulae, inhibits DNA synthesis through covalent mitomycin C-DNA adduct with EC50 values of 0.14μM in PC3 cells.
Mitomycin C is an antibiotic that has demonstrated antitumor activity in preclinical and clinical studies and is widely used to treat various cancers. Mitomycin C is known to act synergistically with capecitabine and irinotecan. Some studies suggested that the combination of 5-FU plus Mitomycin C is more active in vitro than mono-therapy in colorectal cancer. The efficacy of the combination of Mitomycin C with other cytotoxic agents such as capecitabine and raltiterxed for colorectal cancer has been reported.[1]
Mitomycin C not only potentiates TRAIL-induced apoptosis in HCT116 (p53−/−) colon cancer cells but also sensitizes TRAIL-resistant colon cancer cells HT-29 to the cytokine. At a mechanistic level, Mitomycin C downregulates cell survival proteins, including Bcl2, Mcl-1 and Bcl-XL, and upregulates pro-apoptotic proteins including Bax, Bim and the cell surface expression of TRAIL death receptors DR4 and DR5. Besides, the result of cell experiment indicates that Mitomycin C inhibits HT-29 with IC50 of 40 nM. [1,2]
Mitomycin C also plays an effective role in antitumor in vivo. For in vivo experiment, Mitomycin C suppressed tumor growth significantly and did not impact the weight of the mice with TRAIL, indicating that the therapeutic combination of Mitomycin C and TRAIL is well-tolerated and has anti-tumor activity in vivo. [1]
References:
[1]. Cheng H, et al. Mitomycin C potentiates TRAIL-induced apoptosis through p53-independent upregulation of death receptors: evidence for the role of c-Jun N-terminal kinase activation. Cell Cycle. 2012 Sep 1;11(17):3312-23.
[2]. Hodgkinson TJ, et al. Chemical synthesis and cytotoxicity of some azinomycin analogues devoid of the 1-azabicyclo[3.1.0]hexane subunit. Bioorg Med Chem Lett. 2000 Feb 7;10(3):239-41.
Cas No. | 50-07-7 | SDF | |
Synonyms | Ametycine | ||
Chemical Name | ((1aS,8S,8aR,8bS)-6-amino-8a-methoxy-5-methyl-4,7-dioxo-1,1a,2,4,7,8,8a,8b-octahydroazirino[2',3':3,4]pyrrolo[1,2-a]indol-8-yl)methyl carbamate | ||
Canonical SMILES | NC(C1=O)=C(C)C(C2=C1[C@@H](COC(N)=O)[C@]3(OC)N2C[C@H]4[C@@H]3N4)=O | ||
Formula | C15H18N4O5 | M.Wt | 334.33 |
Solubility | ≥ 16.7mg/mL in DMSO | Storage | 4°C, protect from light |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
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Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
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3. All of the above co-solvents are available for purchase on the GlpBio website.
Mitomycin C
Mitomycin C
Mitomycin C
Mitomycin C in the therapy of recurrent esophageal strictures: hype or hope?
Introduction: Esophageal strictures refractory to conservative treatment represent a major problem in children. The application of Mitomycin C to the site of stricture has been introduced, but the experience with this novel approach remains very limited.
Methods: Systematic review of publications on the topical application of Mitomycin C in children with persistent esophageal stricture.
Results: We identified 11 publications including 31 cases. The underlying cause of stricture was caustic ingestion in 19 (61.2%), esophageal surgery in 7 (22.6%), and others in 5 children (16.2%). The median age of the patients was 48 months (range 4 to 276 months). In the majority of cases cotton pledgets soaked in solution of Mitomycin C were applied endoscopically. Various other techniques such as drug-eluting stents were used. Mitomycin C was applied from 1 to 12 times within intervals from 1 to 12 weeks. The concentrations of Mitomycin C varied considerably between 0.1 and 1 mg/mL. After a mean follow-up time of 22 (6 to 60) months complete relief of symptoms was reported for 21 children (67.7%), and 6 (19.4%) had a partial relief. In four children (12.9%) Mitomycin C treatment failed. No direct or indirect adverse effects were reported.
Conclusion: The short-term results of topical Mitomycin C application for refractory esophageal stricture reported in the literature are very encouraging. Prospective studies are mandatory to determine the optimal time points, dosage, and modalities of treatment before a recommendation can be given.
Mitomycin C in corneal refractive surgery
Mitomycin C has played a deciding role in the current revival of excimer laser surface ablation techniques. We review the literature regarding mechanism of action of mitomycin C, histological effects on the cornea, and indications, dose, exposure time, and toxicity of mitomycin C in corneal refractive surgery. Mitomycin C is an alkylating agent with cytotoxic and antiproliferative effects that reduces the myofibroblast repopulation after laser surface ablation and, therefore, reduces the risk of postoperative corneal haze. It is used prophylactically to avoid haze after primary surface ablation and therapeutically to treat pre-existing haze. There is no definite evidence that establishes an exact diopter limit or ablation depth at which to apply prophylactic mitomycin C. It is usually applied at a concentration of 0.2mg/ml (0.02%) for 12 to 120 seconds over the ablated stroma, although some studies suggest that lower concentrations (0.01%, 0.002%) could also be effective in preventing haze when treating low to moderate myopia. This dose of mitomycin C has not been associated with any clinically relevant epithelial corneal toxicity. Its effect on the endothelium is more controversial: two studies report a decrease in endothelial cell density, but the majority of reports suggest that the endothelium is not altered. Regarding mitomycin C's effect on keratocyte population, although animal studies report keratocyte depletion after its use, longer follow-up suggested that the initial keratocyte depletion does not persist over time.
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