L-Carnitine 50% CAS 461-05-2

L-Carnitine 50%

CAS: 461-05-2

SPECIFICATION:

Description: White crystal

Assay: ≥50±1%

Heavy metal: ≤10ppm

Arsenic: ≤2ppm

Molecular Formula C7H16ClNO3
Molar Mass 197.66
Melting Point 197-199°C
Specific Rotation(α) -0.2~+0.2°(20℃/D)(c=5,H2O)
Water Solubility SOLUBLE
Solubility Aqueous Base (Slightly), Methanol (Slightly, Heated), Water (Sparingly, Sonicate
Appearance White powder
Color White to almost white
Merck 14,1849
BRN 4163212
PH 1.8-2.5 (100g/l, H2O)
Storage Condition Store below +30°C.
Stability Hygroscopic
Sensitive Hygroscopic
MDL MFCD00011904
Physical and Chemical Properties Melting point 190-205°C
water-SOLUBLE SOLUBLE
Use For medicine, aquatic feed add nutrients, etc
In vitro study The main role of L-carnitine is to shuttle long-chain fatty acids across the inner mitochondrial membrane. After L-carnitine and acyl-CoA become acyl-carnitine by activation of carnitine palmitoyl transferase (CPT)-I, the transported acyl-carnitine is changed into acyl-CoA by CPT-II in the mitochondria matrix. Palmitoyl-CoA-induced mitochondrial respiration is increased by L-carnitine treatment, and then is accelerated by the presence of ADP. This acceleration is induced by treatment with L-carnitine in a concentration-dependent manner, and is saturated at 5 mM L-carnitine. Pretreatment with L-carnitine augments Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H 2 O 2 -treated HL7702 cells. L-carnitine protects HL7702 cells against H 2 O 2 -induced cell damage through Akt-mediated activation of Nrf2 signaling pathway.
In vivo study L-carnitine is found to down-regulate the ubiquitin proteasome pathway and increase IGF-1 concentrations in animal models. L-carnitine administration for 2 weeks of hindlimb suspension alleviates the decrease in weight and fiber size in the soleus muscle. In addition, L-carnitine suppresses atrogin-1 mRNA expression, which has been reported to play a pivotal role in muscle atrophy. Simultaneous treatment with L-carnitine attenuates the renal fibrosis (which correlated with a reduction of plasma TGF-β1 levels) and the pro-oxidative and proinflammatory status reported in L-NAME groups, with a concomitant increase in the expression of PPAR-γ.

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