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Mitomycin C Sale

(Synonyms: 丝裂霉素 C,Ametycine) 目录号 : GC12353

Mitomycin C是一种抗生素,从链霉菌(Streptomyces Caespitosus)淡紫色链霉菌(Streptomyces Lavendulae)中分离出来。Mitomycin C通过与DNA形成共价mitomycin C-DNA加合物来抑制DNA合成,在PC3细胞中的EC50值为0.14μM

Mitomycin C Chemical Structure

Cas No.:50-07-7

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥441.00
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5mg
¥357.00
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10mg
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实验参考方法

Cell experiment [1, 2]:

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 [1]:

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.

产品描述

Mitomycin C is an antibiotic isolated from Streptomyces Caespitosus or Streptomyces Lavendulae. Mitomycin C inhibits DNA synthesis by forming covalent mitomycin C-DNA adducts with DNA, with an EC50 value of 0.14 μM in PC3 cells.

Mitomycin C can enhance the apoptosis effect induced by TRAIL on HCT116 (p53-/-) colon cancer cells, and can also make TRAIL-resistant colon cancer cells HT-29 sensitive to this cytokine. The IC50 of Mitomycin C on HT-29 cells is 40nM[1,2]. At the mechanistic level, Mitomycin C down-regulates cell survival-related proteins including Bcl2, Mcl-1, and Bcl-XL, and up-regulates the expression of pro-apoptotic proteins such as Bax, Bim, and TRAIL death receptors DR4 and DR5[1,2].

Mitomycin C has shown anti-tumor effects in animal experiments. In in vivo experiments, Mitomycin C significantly inhibited tumor growth and did not affect the body weight of mice under TRAIL treatment, indicating that the therapeutic combination of Mitomycin C and TRAIL was well tolerated in vivo and had antitumor activity[1].

Mitomycin C has demonstrated anti-tumor activity in preclinical and clinical studies and is widely used to treat various cancers. Mitomycin C is known to have synergistic effects with Capecitabine and Irinotecan. Studies have shown that in colorectal cancer, combination therapy of 5-FU or Raltiterxed with Mitomycin C is more effective than single agents[1].

In cell culture experiments, the recommended concentration of Mitomycin C is 0.2-20μg/mL.

Mitomycin C是一种抗生素,从链霉菌(Streptomyces Caespitosus)淡紫色链霉菌(Streptomyces Lavendulae)中分离出来。Mitomycin C通过与DNA形成共价mitomycin C-DNA加合物来抑制DNA合成,在PC3细胞中的EC50值为0.14μM
Mitomycin C可以增强TRAILHCT116p53-/-)结肠癌细胞诱导的凋亡作用,也能够使TRAIL耐药性结肠癌细胞HT-29对这种细胞因子变得敏感。Mitomycin C在HT-29细胞上的IC5040nM[1,2]。在机制水平上,Mitomycin C下调了包括Bcl2Mcl-1Bcl-XL在内的细胞存活相关蛋白,并上调了促凋亡蛋白如BaxBim以及TRAIL死亡受体DR4DR5的表达[1,2]

Mitomycin C动物实验中显示出抗肿瘤效果。在体内实验中,Mitomycin C显著抑制了肿瘤的生长,并且不影响TRAIL治疗下小鼠的体重,这表明Mitomycin CTRAIL的治疗组合在体内耐受性良好并具有抗肿瘤活性[1]

Mitomycin C已在临床前和临床研究中表现出抗肿瘤活性,并广泛用于治疗各种癌症。已知Mitomycin C与卡培他滨(Capecitabine)和伊立替康(Irinotecan)具有协同作用。研究表明,在结直肠癌中,5-FU或雷替曲塞(Raltiterxed)与Mitomycin C的联合治疗比单药更有效[1]

在细胞培养实验,Mitomycin C的建议浓度为0.2-20μg/mL

 

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.

Chemical Properties

Cas No. 50-07-7 SDF
别名 丝裂霉素 C,Ametycine
化学名 ((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
分子式 C15H18N4O5 分子量 334.33
溶解度 ≥ 16.7mg/mL in DMSO 储存条件 4°C, protect from light
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1 mM 2.9911 mL 14.9553 mL 29.9106 mL
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Research Update

Mitomycin C in the therapy of recurrent esophageal strictures: hype or hope?

Eur J Pediatr Surg.2013 Jan 1;31(1):88-94.PMID: 22517516DOI: 10.1055/s-0032-1311695.

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

Surv Ophthalmol.2009 Jul-Aug;54(4):487-502.PMID: 19539836DOI: 10.1016/j.survophthal.2009.04.002.

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.

Mitomycin C and endoscopic sinus surgery: where are we?

Curr Opin Otolaryngol Head Neck Surg2007 Feb;15(1):40-3.PMID: 17211182DOI: 10.1097/MOO.0b013e328011bcae

Purpose of review: Mitomycin C has been used successfully in various ophthalmologic and, more recently, otolaryngologic procedures. Its modulation of fibroblast activity allows for decreased scarring and fibrosis. Several recent trials have examined the efficacy of mitomycin C in reducing synechia and stenosis following endoscopic sinus surgery. Recent findings: Basic science studies using fibroblast cell lines have demonstrated a dose-dependent suppression of activity with the use of mitomycin C. This is further supported by animal studies that have shown lower rates of maxillary ostial restenosis following application of mitomycin C. No human trial, however, has demonstrated a statistically significant impact of mitomycin C on the incidence of postoperative synechia or stenosis following sinus surgery. The limitations of the literature are discussed. Summary: The antiproliferative properties of mitomycin C may theoretically decrease the incidence of synechia and stenosis following endoscopic sinus surgery. Although this is supported by basic science studies and its successful use in other fields, the clinical evidence to date has not shown the application of mitomycin C to be effective in preventing stenosis after endoscopic sinus surgery. Future prospective studies are required before definitive conclusions can be made.

Topical versus interlesional mitomycin C in auricular keloids

Acta Otorrinolaringol Esp (Engl Ed)2021 Sep-Oct;72(5):280-287.PMID: 34535218DOI: 10.1016/j.otoeng.2020.06.006

Background: The Keloid is an elevated fibrous scar that may extend beyond the borders of the original wound. Object: To compare between topical and intralesional mitomycin C in the treatment of auricular keloids. Patients and methods: Prospective randomized study in which 40 patients with auricular keloids were included. The patients were divided into 2 groups, Group I included 32 patients who underwent topical mitomycin C application after the surgical removal of the auricular keloids, while Group II included 8 cases who underwent intra-lesional injection of mitomycin C after surgical removal of the auricular keloids. Results: The two groups showed no significant difference regarding patient or lesion criteria (p>.05). VSS decreased significantly from 10.63 and 11.0 down to 1.38 and 3.0 after treatment in the topical and intra-lesional groups respectively (p<.001). However, greater improvement and satisfaction was detected in the topical group. Conclusion: Both topical and intra-lesional mitomycin C injection are effective methods in managing auricular keloids. However, better VSS scores and patient satisfaction are reported with topical administration.

Intravesical mitomycin C for superficial transitional cell carcinoma

Expert Rev Anticancer Ther 2006 Aug;6(8):1273-82.PMID: 23296407DOI: 10.1586/14737140.6.8.1273.

Intravesical instillation of mitomycin C after a transurethral resection of a bladder tumor constitutes a standard treatment modality in the management of superficial transitional cell carcinoma in the urinary bladder. An immediate instillation of mitomycin C after transurethral resection has been shown to reduce the recurrence rate of superficial transitional cell carcinoma. Intravesical mitomycin C is generally considered to be a safe treatment option, but the past few years have seen the publication of a number of case reports on severe complications following mitomycin C instillation. This article reports on the mode of action, as well as the intravesical effects and current indications for mitomycin C instillation. This review will summarize the oncological benefits of mitomycin C in comparison with other intravesical treatments, such as bacillus Calmette-Guérin, and elucidate the incidence and types of possible complications associated with intravesical mitomycin C chemotherapy.