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554720

Millipore

trans-Retinoic Acid

Potent modulator of growth and differentiation. Inhibits melanocyte adhesion, motility, and growth.

Synonyme(s) :

trans-Retinoic Acid, Tretinoin, ATRA, Vitamin A Acid

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About This Item

Formule empirique (notation de Hill):
C20H28O2
Numéro CAS:
Poids moléculaire :
300.44
Numéro MDL:
Code UNSPSC :
12352106
Nomenclature NACRES :
NA.21

Niveau de qualité

Pureté

≥95% (by assay)

Forme

solid

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze
desiccated (hygroscopic)
protect from light

Couleur

yellow

Solubilité

DMSO: 25 mg/mL

Conditions d'expédition

ambient

Température de stockage

2-8°C

InChI

1S/C20H28O2/c1-15(8-6-9-16(2)14-19(21)22)11-12-18-17(3)10-7-13-20(18,4)5/h6,8-9,11-12,14H,7,10,13H2,1-5H3,(H,21,22)/b9-6+,12-11+,15-8+,16-14+

Clé InChI

SHGAZHPCJJPHSC-YCNIQYBTSA-N

Description générale

Potent modulator of growth and differentiation. Exerts its effects by binding to nuclear retinoic acid receptors (RARs) which directly regulate gene expression. Inhibits melanocyte adhesion, motility, and growth. Has keratolytic activity. Induces differentiation of tumor cells of neural origin. Induces apoptosis in acute promyelocytic carcinoma cells.
Potent modulator of growth and differentiation. Exerts its effects by binding to nuclear retinoic acid receptors (RARs) which directly regulate gene expression. Inhibits melanocyte adhesion, motility, and growth. Has keratolytic activity. Induces differentiation of tumor cells of neural origin. Induces apoptosis in acute promyelocytic carcinoma cells. PROTECT FROM AIR.

Application


  • All-trans-retinoic acid modulates glycolysis via H19 and telomerase: the role of mir-let-7a in estrogen receptor-positive breast cancer cells.: This research reveals how all-trans-retinoic acid influences glycolysis in breast cancer cells by modulating H19 and telomerase, demonstrating its potential in breast cancer therapy (El Habre et al., 2024).

  • Retinoic acid tiers mitochondrial metabolism to Sertoli Cell-Mediated efferocytosis via a non-RAR-dependent mechanism.: The study explores the role of retinoic acid in linking mitochondrial metabolism to efferocytosis in Sertoli cells, providing insights into its non-RAR-dependent mechanisms and potential applications in reproductive biology (Wu et al., 2024).

  • Combined treatment of All-trans retinoic acid with Tamoxifen suppresses ovarian cancer.: This article discusses the synergistic effects of combining all-trans-retinoic acid with tamoxifen in suppressing ovarian cancer, highlighting a promising therapeutic strategy for ovarian cancer patients (Xu et al., 2024).

Conditionnement

Packaged under inert gas

Avertissement

Toxicity: Harmful & Carcinogenic / Teratogenic (E)

Reconstitution

Following reconstitution, store in the refrigerator (4°C). DMSO stock solutions are stable for up to 2 weeks at 4°C.

Autres remarques

Tosi, P., et al. 1994. Leuk. Lymphoma14, 503.
Clagett-Dame, M., et al. 1993. Arch. Biochem. Biophys.300, 684.
Labbaye, C., et al. 1993. Blood81, 475.
Sakashita, A., et al. 1993. Blood81, 1009.
Situ, R., et al. 1993. Dermatology186, 38.
Tini, M., et al. 1993. Genes Develop.7, 295.
Leid, M., et al. 1992. Trends Biochem. Sci.17, 427.
Sharpe, C.R. 1991. Neuron7, 239.
Thaller, C. and Eichele, G. 1990. Nature345, 815.

Informations légales

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

Pictogrammes

Health hazardExclamation markEnvironment

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

Acute Tox. 4 Oral - Aquatic Acute 1 - Aquatic Chronic 1 - Repr. 1B - Skin Irrit. 2

Code de la classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Natalia Moskal et al.
Nature communications, 11(1), 88-88 (2020-01-05)
The accumulation of damaged mitochondria causes the death of dopaminergic neurons. The Parkin-mediated mitophagy pathway functions to remove these mitochondria from cells. Targeting this pathway represents a therapeutic strategy for several neurodegenerative diseases, most notably Parkinson's disease. We describe a

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