Coenzyme A Trilithium Salt – Research Use Only

Coenzyme A Trilithium Salt is a high-purity activated form of Coenzyme A supplied as a 5 mg powder (MW 821.36 g/mol). This essential metabolic cofactor participates in numerous biochemical reactions, including fatty acid β-oxidation, the citric acid cycle, and the biosynthesis of acetylcholine, fatty acids, and polyketides. It is widely used in enzymatic assays, metabolic studies, and as a substrate for acetyl-CoA synthetase and other CoA-dependent enzymes.

Scientific Overview

Coenzyme A (CoA) is a central cofactor in metabolism, functioning as an acyl group carrier in the form of acetyl-CoA, succinyl-CoA, and other acyl-CoAs. The trilithium salt form provides high solubility and stability for in vitro enzymatic reactions. CoA is indispensable for the citric acid cycle, β-oxidation of fatty acids, cholesterol synthesis, and the production of acetylcholine and other neurotransmitters.

This Coenzyme A Trilithium Salt is suitable for:

• In vitro reconstitution of CoA-dependent enzymatic reactions
• Generation of acyl-CoA thioesters for metabolic studies
• Investigation of fatty acid oxidation and energy metabolism pathways
• Acetyl-CoA synthetase and other CoA-utilizing enzyme assays
• Biochemical research involving mitochondrial function and lipid metabolism

Usage & Handling Guidance

Store the lyophilized powder at -20 °C in a desiccated environment. Reconstitute in ultrapure water or appropriate buffer immediately before use. Prepare fresh working solutions or single-use aliquots, as CoA is labile in solution. Keep on ice during experimental procedures.

• Recommended applications: Metabolic enzyme assays, acyl-CoA synthesis, and biochemical pathway studies
• Working concentration: Typically 0.1–1 mM final concentration (optimize for specific assay)
• Solubility: Highly soluble in water; prepare stock solutions as needed
• Handling: Protect from moisture and prolonged exposure to room temperature or alkaline conditions

What You Get

• 5 mg Coenzyme A Trilithium Salt as a high-purity powder
• Molecular weight 821.36 g/mol
• Ready for reconstitution in CoA-dependent enzymatic and metabolic assays
• Biotechnology-grade cofactor manufactured under strict quality controls
• For research use only (RUO)

Why Researchers Choose It

• High-purity Coenzyme A in stable trilithium salt form
• Essential cofactor for fatty acid metabolism, TCA cycle, and acetyl-CoA dependent reactions
• Ideal for in vitro enzyme kinetics and metabolic pathway reconstitution
• Convenient small-quantity powder for precise experimental use
• Manufactured under strict biotechnology-grade standards

Frequently Asked Questions (FAQ)

• What is the role of Coenzyme A?
  CoA acts as an acyl group carrier in central metabolism, forming acetyl-CoA, succinyl-CoA, and other thioesters essential for the citric acid cycle and fatty acid oxidation.
• How should I reconstitute the powder?
  Reconstitute in ultrapure water or neutral buffer immediately before use. Prepare fresh solutions or aliquots to maintain stability.
• What is the recommended working concentration?
  Typically 0.1–1 mM final concentration in enzymatic assays (optimize for your specific reaction).
• Is this product stable in solution?
  CoA is labile in solution; use freshly prepared stocks and keep on ice during experiments.
• Can this be used to generate acetyl-CoA?
  Yes. It is commonly used with acetyl-CoA synthetase or other enzymes to produce acyl-CoA thioesters in vitro.

---

References

• Zhang H, Cuevas J. Sigma receptors inhibit high-voltage-activated calcium channels in rat sympathetic and parasympathetic neurons. J Neurophysiol. 2002 Jun;87(6):2867-79.
• Zhang H, Cuevas J. sigma Receptor activation blocks potassium channels and depresses neuroexcitability in rat intracardiac neurons. J Pharmacol Exp Ther. 2005 Jun;313(3):1387-96.
• Filippov AK, Choi RC, Simon J, Barnard EA, Brown DA. Activation of P2Y1 nucleotide receptors induces inhibition of the M-type K+ current in rat hippocampal pyramidal neurons. J Neurosci. 2006 Sep 6;26(36):9340-8.
• Baldassano S, Zizzo MG, Serio R, Mulè F. Interaction between cannabinoid CB1 receptors and endogenous ATP in the control of spontaneous mechanical activity in mouse ileum. Br J Pharmacol. 2009 Sep;158(1):243-51.
• Sietzen M, Federmann P, Sonnenschein C, Wadepohl H, Ballmann J. Cyclometalated titanium and zirconium complexes stabilised by a new silylmethylene-linked tetradentate triamidophosphine. Dalton Trans. 2016 Feb 21;45(7):3013-23.
• Chen YB, Huang FS, Fen B, Yin JB, Wang W, Li YQ. Inhibitory effects of endomorphin-2 on excitatory synaptic transmission and the neuronal excitability of sacral parasympathetic preganglionic neurons in young rats. Front Cell Neurosci. 2015 May 28;9:206.
• Vrána J, Jambor R, Růžička A, Dostál L. New synthetic strategies leading to [RNPNR](-) anions and the isolation of the [P(Nt-Bu)(3)](3-) trianion. Dalton Trans. 2018 Jun 25;47(25):8434-8441.
• Witkowski G, Szulczyk P. Opioid mu receptor activation inhibits sodium currents in prefrontal cortical neurons via a protein kinase A- and C-dependent mechanism. Brain Res. 2006 Jun 13;1094(1):92-106.
• Han S, Kim JS, Jung BK, Han SE, Nam JH, Kwon YK, Nah SY, Kim BJ. Effects of ginsenoside on pacemaker potentials of cultured interstitial cells of Cajal clusters from the small intestine of mice. Mol Cells. 2012 Mar;33(3):243-9.
• Cuevas J, Adams DJ. M4 muscarinic receptor activation modulates calcium channel currents in rat intracardiac neurons. J Neurophysiol. 1997 Oct;78(4):1903-12.