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890898P

Avanti

DOTMA

Avanti Research™ - A Croda Brand

Synonyme(s) :

1,2-di-O-octadecenyl-3-trimethylammonium propane (chloride salt)

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A propos de cet article

Formule empirique (notation de Hill) :
C42H84ClNO2
Numéro CAS:
104872-42-6
Poids moléculaire :
670.57
MDL number:
MFCD00145456
UNSPSC Code:
12352211
NACRES:
NA.25
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assay

>99% (TLC)

form

powder

packaging

pkg of 2 × 100 mg (890898P-200mg), pkg of 1 × 25 mg (890898P-25mg)

manufacturer/tradename

Avanti Research™ - A Croda Brand

application(s)

advanced drug delivery

lipid type

cationic lipids
transfection

shipped in

dry ice

storage temp.

−20°C

SMILES string

[H]C(C[N+](C)(C)C)(OCCCCCCCC/C=C\CCCCCCCC)COCCCCCCCC/C=C\CCCCCCCC.[Cl-]

InChI key

LDGWQMRUWMSZIU-LQDDAWAPSA-M

Application

DOTMA is suitable for use as a building block of miRNA delivery system and in the preparation.

Biochem/physiol Actions

DOTMA is a cationic lipid, used as a non-viral vector for gene therapy. It exhibits effective in vitro and in vivo gene transfection. DOTMA induces a positive charge on the liposomes and thus promotes efficient liposome - cell membrane interaction.

Packaging

5 mL Clear Glass Sealed Ampule (890898P-200mg)
5 mL Clear Glass Sealed Ampule (890898P-25mg)

Legal Information

Avanti Research is a trademark of Avanti Polar Lipids, LLC

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11 - Combustible Solids

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Consulter la Bibliothèque de documents

Yun Wu et al.
Molecular therapy. Nucleic acids, 2, e84-e84 (2013-04-18)
MicroRNA-29b (miR-29b) expression has been shown to be reduced in non-small-cell lung cancer (NSCLC) tissues. Here, we have identified the oncogene cyclin-dependent protein kinase 6 (CDK6) as a direct target of miR-29b in lung cancer. We hypothesized that in vivo
The use of cationic microbubbles to improve ultrasound-targeted gene delivery to the ischemic myocardium
Sun L, et al.
Biomaterials, 34(8), 2107-2116 (2013)
Jinhong Meng et al.
Scientific reports, 10(1), 1046-1046 (2020-01-25)
P53 mutations are responsible for drug-resistance of tumour cells which impacts on the efficacy of treatment. Alternative tumour suppressor pathways need to be explored to treat p53- deficient tumours. The E3 ubiquitin ligase, ITCH, negatively regulates the tumour suppressor protein
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