(±)-Carnitine (chloride)

CAS No. : 461-05-2

(Synonyms: DL-Carnitine chloride)

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Cat. No. : HY-B1453
M.Wt: 197.66
Formula: C7H16ClNO3
Purity: >98 %
Solubility: H2O : ≥ 100 mg/mL (505.92 mM); DMSO : 25 mg/mL (126.48 mM; Need ultrasonic)
Introduction of 461-05-2 :

(±)-Carnitine chloride exists in two isomers, known as D and L. L-carnitine plays an essential role in the β-oxidation of fatty acids and also shows antioxidant, and anti-inflammatory activities. In Vitro: 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[1]. Pretreatment with L-carnitine augments Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H2O2-treated HL7702 cells. L-carnitine protects HL7702 cells against H2O2-induced cell damage through Akt-mediated activation of Nrf2 signaling pathway[2]. In Vivo: 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[3]. 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[4].

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