DL-Carnitine HCL JPC2002
CAS: 461-05-2
SPECIFICATION:
Description: White crystal
Assay: ≥100±2%
Melting point:: 194~198°C
Loss on drying: ≤ 1.0%
Residue on ignition: ≤ 0.5%
NH4+:≤0.1%
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. |