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475820

Millipore

Mitomycin C, Streptomyces caespitosus, Carrier-Free

Antibiotic and carcinostatic agent. Inhibits DNA synthesis by cross-linking DNA at guanine and adenine residues; disrupts base pairing. Induces apoptosis in gastric cancer cells.

Synonyme(s) :

Mitomycin C, Streptomyces caespitosus, Carrier-Free, Mitocin C, MMC

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About This Item

Formule empirique (notation de Hill):
C15H18N4O5
Numéro CAS:
50-07-7
Poids moléculaire :
334.33
Numéro MDL:
MFCD00078109
Code UNSPSC :
12352200

Niveau de qualité

100

Essai

≥95% (HPLC)

Forme

solid

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze
protect from light

Couleur

purple

Solubilité

water: <1 mg/mL
methanol: 5 mg/mL

Conditions d'expédition

ambient

Température de stockage

2-8°C

InChI

1S/C15H18N4O5/c1-5-9(16)12(21)8-6(4-24-14(17)22)15(23-2)13-7(18-13)3-19(15)10(8)11(5)20/h6-7,13,18H,3-4,16H2,1-2H3,(H2,17,22)/t6-,7+,13+,15-/m1/s1

Clé InChI

NWIBSHFKIJFRCO-WUDYKRTCSA-N

Description générale

Antibiotic and carcinostatic agent. Inhibits DNA synthesis by cross-linking DNA at guanine and adenine residues; disrupts base pairing. Induces apoptosis in gastic cancer cells. Blocks the cell cycle at the G2 phase.
Antibiotic and carcinostatic agent. Inhibits DNA synthesis by cross-linking DNA at guanine and adenine residues; disrupts base pairing. Induces apoptosis in gastric cancer cells. Blocks the cell cycle at the G2 phase. Potency: ≥970 µg/mg.

Actions biochimiques/physiologiques

Potency: ≥ 970 μg/mg mitomycin C

Avertissement

Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Autres remarques

Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.
Kryt, F.A., et al. 1996. Blood 89, 938.
Schwartz, G.K., et al. 1995. J. Natl. Cancer Inst. 87, 1394.
Folnan, R.S., 1993. Oncology 50, 24.
Tomasz, M., et al. 1987. Science 235, 1204.

Informations légales

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Pictogrammes

Skull and crossbonesHealth hazard
GHS06,GHS08

Mention d'avertissement

Danger

Mentions de danger

H300,H351

Classification des risques

Acute Tox. 2 Oral - Carc. 2

Code de la classe de stockage

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Fangzhou Lou et al.
British journal of pharmacology, 181(8), 1290-1307 (2023-09-26)
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Arvind Panday et al.
Molecular cell, 81(11), 2428-2444 (2021-04-22)
Repair pathway "choice" at stalled mammalian replication forks is an important determinant of genome stability; however, the underlying mechanisms are poorly understood. FANCM encodes a multi-domain scaffolding and motor protein that interacts with several distinct repair protein complexes at stalled
Romie Angelo G Azur et al.
PloS one, 19(5), e0300413-e0300413 (2024-05-13)
Castration-resistant prostate cancer (CRPC) is associated with resistance to androgen deprivation therapy, and an increase in the population of neuroendocrine (NE) differentiated cells. It is hypothesized that NE differentiated cells secrete neuropeptides that support androgen-independent tumor growth and induce aggressiveness
Yuchuan Li et al.
Cancer cell international, 23(1), 276-276 (2023-11-18)
Despite therapeutic advances, the prognosis of pancreatic ductal adenocarcinoma (PDAC) remains extremely poor. Metabolic reprogramming is increasingly recognized as a key contributor to tumor progression and therapy resistance in PDAC. One of the main metabolic changes essential for tumor growth

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