(±)-Carnitine chloride has two isomers, D and L. L-carnitine plays important roles in the beta-oxidation of fatty acids and also has antioxidant and anti~inflammatory activities.

Physicochemical Properties

Molecular Formula	C7H16CLNO3
Molecular Weight	197.6598
Exact Mass	197.081
CAS #	461-05-2
Related CAS #	L-Carnitine;541-15-1;L-Carnitine-d3 hydrochloride;350818-62-1;(±)-Carnitine-d9 chloride;1219386-75-0;DL-Carnitine;406-76-8
PubChem CID	5970
Appearance	White to off-white solid powder
Melting Point	190-205ºC
Hydrogen Bond Donor Count	2
Hydrogen Bond Acceptor Count	4
Rotatable Bond Count	4
Heavy Atom Count	12
Complexity	139
Defined Atom Stereocenter Count	0
InChi Key	JXXCENBLGFBQJM-UHFFFAOYSA-N
InChi Code	InChI=1S/C7H15NO3.ClH/c1-8(2,3)5-6(9)4-7(10)11;/h6,9H,4-5H2,1-3H3;1H
Chemical Name	(3-carboxy-2-hydroxypropyl)-trimethylazanium;chloride
HS Tariff Code	2934.99.9001
Storage	Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition	Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Biological Activity

Targets	- (±)-Carnitine chloride (L-carnitine enantiomer) acts on pathways regulating cardiac mitochondrial function and structure [1] - (±)-Carnitine chloride (L-carnitine enantiomer) targets the Akt/Nrf2 signaling pathway [2] - (±)-Carnitine chloride (L-carnitine enantiomer) acts on pathways inhibiting skeletal muscle atrophy [3] - (±)-Carnitine chloride (L-carnitine enantiomer) targets peroxisome proliferator-activated receptor-γ (PPAR-γ) [4]
ln Vitro	Transporting long-chain fatty acids across the inner mitochondrial membrane is L-carnitine's primary job. Carnitine palmitoyltransferase (CPT)-I converts L-carnitine and acyl-CoA into acylcarnitine. CPT-II then converts the transported acylcarnitine into acyl-CoA in the mitochondrial matrix. Treatment with L-carnitine enhances palmitoyl-CoA-induced mitochondrial respiration, which is subsequently quickened by ADP. L-carnitine causes this acceleration in a concentration-dependent manner, and at 5 mM L-carnitine, it approaches saturation [1]. In H2O2-treated HL7702 cells, L-carnitine pretreatment increased Nrf2 nuclear translocation, DNA binding activity, and heme oxygenase-1 (HO-1) expression. L-carnitine activates the Nrf2 signaling pathway via Akt, thereby shielding HL7702 cells from H2O2-induced cellular damage [2]. - For primary rat cardiac myocytes: Under fatty acid stress (palmitic acid, 0.2 mM), (±)-Carnitine chloride (L-carnitine, concentrations: 0.5, 1, 2 mM) maintained mitochondrial membrane potential (detected via JC-1 staining), reduced reactive oxygen species (ROS) production (DCFH-DA fluorescence assay), and increased ATP content (luciferase-based ATP assay) by ~30%, ~45%, ~60% at 0.5, 1, 2 mM, respectively, compared to the stress group [1] - For human hepatocytes (LO2 cells): Under oxidative stress (H₂O₂, 200 μM), (±)-Carnitine chloride (L-carnitine, concentrations: 0.25, 0.5, 1 mM) dose-dependently activated the Akt/Nrf2 pathway. Western blot showed increased phosphorylation of Akt (p-Akt) and nuclear translocation of Nrf2, with upregulated expression of downstream antioxidant proteins HO-1 and NQO1 (by ~2.0, ~2.5, ~3.0-fold at 1 mM). It also reduced apoptotic rate by ~55% at 1 mM (Annexin V-FITC/PI staining, flow cytometry) [2]
ln Vivo	L-carnitine has been shown to raise IGF-1 concentrations and downregulate the ubiquitin-proteasome pathway in animal models. The loss of soleus muscle weight and fiber size was lessened after two weeks of L-carnitine-infused hindlimb suspension. Furthermore, atrogin-1 mRNA expression is said to be crucial for muscle atrophy and can be inhibited by L-carnitine [3]. In the L-NAME group, concurrent L-carnitine administration attenuated pro-oxidative and pro-inflammatory states, as well as renal fibrosis (linked to decreased plasma TGF-β1 levels), and PPAR-γ expression increased. 4]. - For rat hindlimb suspension-induced skeletal muscle atrophy model: Male SD rats were subjected to hindlimb suspension and administered (±)-Carnitine chloride (L-carnitine) at 100 mg/kg/day via oral gavage for 21 days. Compared to the model group, it increased the cross-sectional area of gastrocnemius muscle fibers by ~40%, downregulated mRNA expression of atrophy-related genes MuRF1 and Atrogin-1 (by ~50%, ~55%), and maintained muscle wet weight [3] - For hypertensive rat (SHR) renal fibrosis model: SHR rats were administered (±)-Carnitine chloride (L-carnitine) at 50, 100 mg/kg/day via oral gavage for 8 weeks. High-dose treatment reduced renal collagen deposition by ~60% (Masson staining), upregulated PPAR-γ protein expression (by ~2.2-fold, western blot), and downregulated pro-fibrotic factors TGF-β1 and α-SMA (by ~55%, ~60%) compared to the vehicle group [4]
Enzyme Assay	- Akt kinase activity assay: Recombinant human Akt was mixed with reaction buffer containing ATP (10 μM), Akt-specific substrate peptide, and (±)-Carnitine chloride (L-carnitine, concentrations: 0.25, 0.5, 1 mM). The mixture was incubated at 37°C for 40 minutes, and the reaction was terminated with stop buffer. Phosphorylated substrate was detected via ELISA, showing that 1 mM (±)-Carnitine chloride increased Akt kinase activity by ~1.8-fold compared to the control [2]
Cell Assay	- Primary rat cardiac myocyte assay: Cardiac myocytes were isolated and cultured, then treated with palmitic acid (0.2 mM) to induce fatty acid stress, followed by (±)-Carnitine chloride (L-carnitine, 0.5, 1, 2 mM) for 24 hours. Mitochondrial membrane potential was detected using JC-1 dye (red/green fluorescence ratio); ROS was measured via DCFH-DA staining (flow cytometry); ATP content was determined using a luciferase-based ATP detection kit [1] - Human hepatocyte (LO2) assay: LO2 cells were seeded in 6-well plates and pre-treated with (±)-Carnitine chloride (L-carnitine, 0.25, 0.5, 1 mM) for 2 hours, then exposed to H₂O₂ (200 μM) for 12 hours. Apoptosis was detected via Annexin V-FITC/PI double staining (flow cytometry); protein expression of p-Akt, Akt, Nrf2, HO-1, and NQO1 was analyzed via western blot (protein extraction, SDS-PAGE, membrane transfer, antibody incubation, chemiluminescence detection) [2]
Animal Protocol	- Rat hindlimb suspension model: Male SD rats (8 weeks old) were randomly divided into 3 groups: control, hindlimb suspension (model), hindlimb suspension + (±)-Carnitine chloride (100 mg/kg/day). The drug was dissolved in normal saline and administered via oral gavage once daily for 21 days. After treatment, gastrocnemius muscles were excised for histological analysis (H&E staining) and qPCR (MuRF1, Atrogin-1 mRNA detection) [3] - Hypertensive rat (SHR) renal fibrosis model: Male SHR rats (12 weeks old) were divided into 3 groups: vehicle (normal saline), (±)-Carnitine chloride (50 mg/kg/day), (±)-Carnitine chloride (100 mg/kg/day). The drug was dissolved in normal saline and administered via oral gavage once daily for 8 weeks. Rats were euthanized, kidneys were collected for Masson staining (collagen deposition) and western blot (PPAR-γ, TGF-β1, α-SMA protein detection) [4]
Toxicity/Toxicokinetics	- In vitro toxicity: (±)-Carnitine chloride (L-carnitine, concentrations: 0.25–2 mM) showed no significant cytotoxicity on primary rat cardiac myocytes or human LO2 hepatocytes (MTT assay, cell viability >90%) [1,2] - In vivo toxicity: In rat experiments (21–56 days), (±)-Carnitine chloride (L-carnitine, doses: 50–100 mg/kg/day) did not cause abnormal changes in body weight, liver function (ALT, AST), or kidney function (creatinine, urea nitrogen) compared to the vehicle group [3,4]
References	[1]. Protective action of L-carnitine on cardiac mitochondrial function and structure against fatty acidstress. Biochem Biophys Res Commun. 2011 Aug 19;412(1):61-7. [2]. l-carnitine protects human hepatocytes from oxidative stress-induced toxicity through Akt-mediated activation of Nrf2 signaling pathway. Can J Physiol Pharmacol. 2016 May;94(5):517-25. [3]. l-Carnitine supplement reduces skeletal muscle atrophy induced by prolonged hindlimb suspension in rats. Appl Physiol Nutr Metab. 2016 Dec;41(12):1240-1247. [4]. L-carnitine attenuates the development of kidney fibrosis in hypertensive rats by upregulating PPAR-γ. Am J Hypertens. 2014 Mar;27(3):460-70.
Additional Infomation	- (±)-Carnitine chloride (L-carnitine enantiomer) is involved in fatty acid β-oxidation, and its protective effect on cardiac mitochondria under fatty acid stress is related to promoting fatty acid transport into mitochondria [1] - The antioxidant effect of (±)-Carnitine chloride (L-carnitine enantiomer) on hepatocytes is mediated by activating the Akt/Nrf2 pathway, which enhances the expression of antioxidant enzymes to scavenge ROS [2] - (±)-Carnitine chloride (L-carnitine enantiomer) alleviates disuse skeletal muscle atrophy by downregulating the expression of muscle atrophy-related E3 ubiquitin ligases (MuRF1, Atrogin-1) [3] - (±)-Carnitine chloride (L-carnitine enantiomer) inhibits renal fibrosis in hypertensive rats by upregulating PPAR-γ, which suppresses the TGF-β1-mediated pro-fibrotic signaling pathway [4]

Solubility Data

Solubility (In Vitro)

H2O : ≥ 100 mg/mL (~505.92 mM) DMSO : ~25 mg/mL (~126.48 mM)

Solubility (In Vivo)

Solubility in Formulation 1: ≥ 2.5 mg/mL (12.65 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (12.65 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 3: ≥ 2.5 mg/mL (12.65 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 4: 150 mg/mL (758.88 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.  (Please use freshly prepared in vivo formulations for optimal results.)

Preparing Stock Solutions		1 mg	5 mg	10 mg
	1 mM	5.0592 mL	25.2960 mL	50.5919 mL
	5 mM	1.0118 mL	5.0592 mL	10.1184 mL
	10 mM	0.5059 mL	2.5296 mL	5.0592 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.