GLPBio

Gemcitabine

Catalog No.: GC16805Purity:>99.00%Synonyms: DDFC, LY 188011, NSC 613327
COASDSData Sheet
La gemcitabine (LY 188011) est un antimétabolite analogue du nucléoside pyrimidique et un agent antinéoplasique. La gemcitabine inhibe la synthèse et la réparation de l'ADN, entraÎnant l'autophagie et l'apoptose.

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Gemcitabine
Cas No.: 95058-81-4
10mM (in 1mL DMSO)In Stock
$37.00
1
100mgIn Stock
$35.00
1
Tel: (909) 407-4943 / (909) 689-7124Email: sales@glpbio.com

Citations

6 publicationsPublications de chercheurs utilisant ce produit

Description

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].

References:
[1].  Karnitz LM, Flatten KS, Wagner JM, et al. Gemcitabine-induced activation of checkpoint signaling pathways that affect tumor cell survival. Mol Pharmacol, 2005, 68(6): 1636-1644.
[2].  Ando T, Ichikawa J, Okamoto A, et al. Gemcitabine inhibits viability, growth, and metastasis of osteosarcoma cell lines. J Orthop Res, 2005, 23(4): 964-969.
[3].  Clouser CL, Holtz CM, Mullett M, et al. Analysis of the ex vivo and in vivo antiretroviral activity of gemcitabine. PLoS One, 2011, 6(1): e15840.

Protocole (Protocol)

Cell experiment [1]:

Cell lines

HeLa cells, K562 cells, HOS and MG63 cell lines.

Preparation method

The solubility of this compound in DMSO﹥10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

100 nM gemcitabine for 3 h in HeLa cells for immunofluorescence, 500 nM gemcitabine for 6 h for SDS-PAGE

Applications

In Hela cells and K562 cells, gemcitabine activated both the ATR/Chk1 and ATM/Chk2 signaling pathways. (ATR: ataxia-telangiectasia mutated and Rad3-related kinase; Chk: checkpoint kinase; ATM: ataxia-telangiectasia mutated kinase). 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.
Animal experiment [2]:

Animal models

Female C57BL/6 mice infected with LP-BM5 MuLV

Dosage form

1, 2, 4 mg/kg/day for 8 week by injection.

Application

Mice treated with 1 or 2 mg/kg/day had an average ratio of spleen to body weight that was significantly lower than the infected with virus, untreated mice. Treatment with gemcitabine decreased MAIDS associated lesions in the lymph nodes. IgM levels from mice treated with 2 mg/kg/day of gemcitabine were significantly lower than that seen in the uninfected animals. Gemcitabine decreased provirus levels.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Karnitz LM, Flatten KS, Wagner JM, et al. Gemcitabine-induced activation of checkpoint signaling pathways that affect tumor cell survival. Mol Pharmacol, 2005, 68(6): 1636-1644.

[2] Ando T, Ichikawa J, Okamoto A, et al. Gemcitabine inhibits viability, growth, and metastasis of osteosarcoma cell lines. J Orthop Res, 2005, 23(4): 964-969.

[3] Clouser CL, Holtz CM, Mullett M, et al. Analysis of the ex vivo and in vivo antiretroviral activity of gemcitabine. PLoS One, 2011, 6(1): e15840.

Documents produit (Product Documents)

Purity:>99.00%Appearance:A solid
COASDSData Sheet

Données biologiques (Biological Data)

1 / 1

Propriétés chimiques (Chemical Properties)

N° CAS
95058-81-4
Synonymes
DDFC, LY 188011, NSC 613327
Nom chimique
4-amino-1-[(2R,4R,5R)-3,3-difluoro-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one
SMILES
C1=CN(C(=O)N=C1N)C2C(C(C(O2)CO)O)(F)F
Formule moléculaire
C9H11F2N3O4
Masse moléculaire
263.2
Solubilité
DMSO: 53 mg/mL (201.37 mM); H2O : 7mg/mL (23.75 mM; ultrasonic and warming and heat to 60°C)
Conservation
Store at -20°C, protect from light
Conseils généraux
Choisissez un solvant adapté selon les données de solubilité du produit. Après préparation, répartissez la solution mère en aliquotes afin d’éviter les cycles répétés de congélation-décongélation.
Utilisez les solutions mères dans les 6 mois si elles sont conservées à -80°C, ou dans le mois si elles sont conservées à -20°C.
Pour améliorer la solubilité, réchauffez le tube à 37°C et soniquez-le pendant une durée appropriée.
Conditions d’expédition
Les échantillons d’évaluation sont expédiés avec des blocs réfrigérants. Les autres formats sont expédiés à température ambiante ou, sur demande, avec des blocs réfrigérants.

Calculateurs (Calculators)Molarité / Dilution / Masse moléculaire / Conversion d’unités / Formulation in vivo / Solubilité

g/mol

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