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N-Nitroso-N-methylurea

MCE China：N-Nitroso-N-methylurea

Brand：MedChemExpress (MCE)

Cat. No.HY-34758

CAS：684-93-5

Purity：98.0%

Storage：-20°C, protect from light, stored under nitrogen *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：N-Nitroso-N-methylurea (NMU;MNU;NMH) is a potent carcinogen, mutagen and teratogenand. N-Nitroso-N-methylurea is a direct-acting alkylating agent that interacts with DNA. N-Nitroso-N-methylurea targets multiple animal organs to cause various cancer and/or degenerative disease. N-Nitroso-N-methylurea is also a precursor in the synthesis of diazomethane.

In Vitro：N-Nitroso-N-methylurea (NMU; 5 μM) treatment increases the cellular NF-κB activity in human malignant keratinocytes. N-Nitroso-N-methylurea also increases the amount of I-κBα phosphorylation[5].

In Vivo：N-Methyl-N-nitrosourea (MNU) can be used to create models of gastric cancer and breast cancer[6][7]. .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of Gastric Cancer[6] Background N-Methyl-N-nitrosourea (MNU) is a direct-acting alkylating agent that interacts with DNA. Accumulation of mutations may enhance cancer risk in target organs or cause cell death in susceptible tissues or cells when excessive DNA damage is not repaired. MNU targets various organs in a variety of animal species[2]. Specific Mmodeling Methods Rat: albino Wistar • male • 5-6-week-old; 110-140 gAdministration: 100 mg/kg • ig • thrice in a week for 16 weeks Note (1) Dissolved in citrate buffer and 5% saline thrice in a week via intragastric route for 16 weeks.(2) The level of cancer induction was identified by specific biochemical markers such as serum gastrin level, TBARS, and glutathione followed by histopathological analysis at two-time periods for 8 and 16 week. Modeling Indicators Individual phenotypic changes: showed a significant decrease in body weight, water intake, and feed intake.Molecular changes: increased the mean serum gastrin level, increased level of lipid peroxidation and decreased reduced glutathione level in gastric tissues.Tissue changes: MNU-induced rats disclosed that the non-glandular stomach epithelium was hypertrophic with vacuolations and orthokeratotic hyperkeratosis after 16 wk of MNU induction but vacuolations and hyperkeartosis were not that much observed at 8 wk of MNU induction. Correlated Product(s): / Opposite Product(s): Cancer Models .f12{ font-size: 12px; } .fwb{ font-weight: bold; } .lh22{ line-height: 22px;; } .lh23 { line-height: 23px; } .pl13{ padding-left: 13px;; } .part { margin-top: 18px; } .mold-first-tit { width: 100%; height: 44px; line-height: 44px; background: #F9F7FB; border-bottom: 1px solid #EBE4F6; padding-left: 16px; box-sizing: border-box; margin-bottom: 17px; } .mold-second-tit:before { content:""; width: 6px; height: 6px; display: inline-block; border-radius: 50%; background: rgba(255,102,0,0.4); margin-right: 12px; position: relative; top: -3px; } .lft-border { border-left: 1px dotted #EBE4F6; padding-right: 12px; margin-left: 3px; box-sizing: border-box; padding-bottom: 12px; } /* .part .dec:last-child { border-bottom: 0; } */ .dec { margin: 10px 15px 0; padding-bottom: 10px; border-bottom: 1px dashed #EBE4F6; } .btm-border { border-left: 1px dashed #EBE4F6; } .text-bg { margin-top: 10px; background: #FFFBF1; padding: 14px; border-bottom: 0; position: relative; } .text-note-bg { margin-top: 10px; background: #FFFDF7; padding: 12px; border-bottom: 0; position: relative; } .text-note { width: 51px; height: 20px; line-height: 20px; background: #FFE2AA; text-align: center; border-radius: 0 0 8px 0; position: absolute; top: 0; left: 0; } .text-note-dec { margin-top: 15px;; } Induction of Breast Cancer[7] Background DNA Damage: After entering the body, MNU can be metabolically activated to form active nitrosyl compounds. These compounds react with DNA molecules, causing DNA strand breaks or base modifications, particularly alkylations such as O6-methylguanine. If not repaired, this type of damage can lead to mutations during cell division. Gene Mutations: Due to the aforementioned DNA damage not being effectively repaired, errors may occur when cells replicate DNA, resulting in gene mutations. These mutations can affect key processes such as cell cycle regulation, apoptosis signaling pathways, and DNA repair mechanisms, thereby promoting tumor initiation and progression. Uncontrolled Cell Proliferation: Gene mutations induced by MNU can activate oncogenes or inactivate tumor suppressor genes, disrupting normal cell growth control mechanisms. This results in cells losing their responsiveness to external growth inhibitory signals, leading to abnormal proliferation. Pro-inflammatory Environment: Research has shown that MNU may also promote tumor development by altering the local microenvironment, such as increasing the expression of inflammatory factors. A chronic inflammatory state is considered an important factor in tumor development, as it can promote angiogenesis, epithelial-mesenchymal transition (EMT), and other processes that favor cancer progression. Immune Evasion: Long-term exposure to MNU may impair the body's immune surveillance function, allowing tumor cells to evade recognition and elimination by the host immune system, further promoting tumor growth and metastasis. Specific Mmodeling Methods Rat: Albino Wistar • female • 35-day-old; 110-140 gAdministration: 50 mg/kg • ip • at 50, 65, and 80 days of age Note Modeling Indicators Molecular changes: increased cyclin D1 expression, and showed p21Cip1 overexpression.Tissue changes: observed breast tumors, and increased the mean volumes of tumors. Correlated Product(s): / Opposite Product(s): Cancer Models

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References：

[1]. Gullino PM, et al. N-nitrosomethylurea as mammary gland carcinogen in rats. J Natl Cancer Inst. 1975 Feb;54(2):401-14.  [Content Brief]

[2]. Tsubura A, et al. Review: Animal models of N-Methyl-N-nitrosourea-induced mammary cancer and retinal degeneration with special emphasis on therapeutic trials. In Vivo. 2011 Jan-Feb;25(1):11-22.  [Content Brief]

[3]. Johnson EM, et al. Effects of N-nitroso-N-methylurea on enzymatic ontogeny associated with teratogenesis. Teratology. 1968 May;1(2):179-91.  [Content Brief]

[4]. Silvia Garbarino, et al. One-pot synthesis of α-haloketones employing a membrane-based semibatch diazomethane generator. Journal of Flow Chemistry volume 6, pages211-217(2016).

[5]. Moon KY. N-nitroso-N-methylurea and N-nitroso-N-ethylurea induce upregulation of cellular NF-kappa B activity through protein kinase C-dependent pathway in human malignant keratinocytes. Arch Pharm Res. 2010 Jan;33(1):133-9.  [Content Brief]

[6]. Mansingh DP, et al. Palliative Role of Aqueous Ginger Extract on N-Nitroso-N-Methylurea-Induced Gastric Cancer. Nutr Cancer. 2020;72(1):157-169.  [Content Brief]

[7]. Ashrafi M, et al. Effect of Crocin on Cell Cycle Regulators in N-Nitroso-N-Methylurea-Induced Breast Cancer in Rats. DNA Cell Biol. 2015 Nov;34(11):684-91.  [Content Brief]