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SML2035

Sigma-Aldrich

Didox

≥98% (HPLC)

Synonym(e):

3,4-Dihydroxybenzohydroxamic acid, 3,4-Dihydroxyphenylhydroxamic acid, BRN 2096682, CCRIS 7909, N,3,4-Trihydroxybenzamide, NSC 324360, NSC-324360, VF 147

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About This Item

Empirische Formel (Hill-System):
C7H7NO4
CAS-Nummer:
69839-83-4
Molekulargewicht:
169.13
MDL-Nummer:
MFCD01667810
UNSPSC-Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

powder

Farbe

white to light brown

Löslichkeit

DMSO: 2 mg/mL, clear

Lagertemp.

−20°C

SMILES String

OC1=CC=C(C(NO)=O)C=C1O

InChI

1S/C7H7NO4/c9-5-2-1-4(3-6(5)10)7(11)8-12/h1-3,9-10,12H,(H,8,11)

InChIKey

QJMCKEPOKRERLN-UHFFFAOYSA-N

Biochem./physiol. Wirkung

Didox is a ribonucleotide reductase (RNR) inhibitor that inhibits proliferation of and decreased secretion of cytokines IL-6, IFN-g, TNF-a, IL-2, IL-13, IL-10 and IL-4. Didox inhibits proliferation of tamoxifen-resistant breast cancer cells. Didox is an antioxidant that potentiates the cytotoxic profile of doxorubicin.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Ahmed M Al-Abd et al.
European journal of pharmacology, 718(1-3), 361-369 (2013-09-12)
The use of adjuvant therapies in cancer treatment is rationalized by potentiating the efficacy and/or protecting from the major side effects of chemotherapeutics. Didox, besides its antioxidant properties, is an inhibitor for DNA synthesis and repair which might recommend its
Sahar A Khaleel et al.
Scientific reports, 6, 36855-36855 (2016-11-15)
Doxorubicin (DOX) has limited efficacy in colorectal cancer due to multi-drug resistance. Resveratrol (RES) and didox (DID) are polyhydroxyphenols with potential chemosensitizing effects. Herein, we assessed the chemomodulatory effects of RES and DID to DOX in colorectal cancer cells. Equitoxic
Khyati N Shah et al.
Molecular cancer research : MCR, 12(3), 394-407 (2013-12-24)
Acquired tamoxifen resistance develops in the majority of hormone-responsive breast cancers and frequently involves overexpression of the PI3K/AKT axis. Here, breast cancer cells with elevated endogenous AKT or overexpression of activated AKT exhibited tamoxifen-stimulated cell proliferation and enhanced cell motility.

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