Pyruvic acid does not have a specific molecular target in the context of pharmacology; rather, it is a key metabolite and a central hub in cellular metabolism. As the end product of glycolysis, it is the substrate for several critical enzymes, including pyruvate dehydrogenase (which converts it to acetyl-CoA for entry into the citric acid cycle), lactate dehydrogenase (which converts it to lactate under anaerobic conditions), and pyruvate carboxylase (which converts it to oxaloacetate for gluconeogenesis). Its role as a substrate for these enzymes makes it a crucial regulator of energy production and metabolic flux. It also acts as a potent antioxidant, capable of scavenging reactive oxygen species (ROS). Pyruvic acid is a conjugate acid of pyruvate, the anion form that predominates at physiological pH.

The primary in vitro activity of pyruvic acid is as a substrate and intermediate in metabolic reactions. In cell-free systems, it is used as a substrate to study the activity of enzymes such as pyruvate dehydrogenase, lactate dehydrogenase, and alanine aminotransferase. Its ability to scavenge reactive oxygen species (ROS) has also been demonstrated in vitro, making it a molecule of interest in oxidative stress research. It has a density of 1.265 g/mL and a refractive index of 1.424. Its high solubility in water and other polar solvents facilitates its use in various biochemical assays. Pyruvic acid is also used as a standard in analytical chemistry and as a precursor in the synthesis of other compounds.

In vivo, pyruvic acid plays a central role in energy metabolism. It is a key intermediate in the metabolic pathways that convert carbohydrates, fats, and proteins into energy. It is produced in the cytoplasm during glycolysis and is then transported into the mitochondria, where it is converted to acetyl-CoA by the pyruvate dehydrogenase complex. Acetyl-CoA then enters the citric acid cycle, leading to the production of ATP, the cell's primary energy currency. Pyruvic acid is also a precursor for the synthesis of glucose (gluconeogenesis) and amino acids. Its levels in the blood can be altered in various metabolic disorders, such as diabetes and lactic acidosis. Pyruvic acid is also a natural product and a secondary metabolite.

In vitro enzyme assays using pyruvic acid are fundamental to the study of metabolism. The activity of pyruvate dehydrogenase (PDH) can be measured by incubating the enzyme with pyruvic acid, coenzyme A (CoA), and NAD⁺. The production of acetyl-CoA and NADH is monitored spectrophotometrically. Similarly, the activity of lactate dehydrogenase (LDH) can be measured by monitoring the conversion of pyruvic acid to lactate in the presence of NADH. The decrease in absorbance at 340 nm due to the oxidation of NADH is measured. These assays are essential for understanding metabolic regulation and for screening compounds that may affect these pathways.

In vitro cell-based assays using pyruvic acid are performed to study its effects on cellular metabolism and energy production. Cells are cultured in a medium containing glucose, and the production of pyruvic acid and lactate is measured. The effect of various compounds on pyruvate metabolism can be assessed by measuring the levels of pyruvate, lactate, and other metabolites in the cell culture medium. Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) can be measured using a Seahorse analyzer to assess mitochondrial function and glycolysis. These assays are crucial for studying metabolic diseases and for screening potential therapeutic agents.

In vivo animal studies with pyruvic acid are often conducted to study its effects on metabolism and energy production. The compound can be administered to animals via intravenous or intraperitoneal injection, and its effects on blood glucose, lactate, and other metabolites are measured. It is used in models of metabolic disorders, such as diabetes and obesity, to study the role of pyruvate metabolism in disease pathogenesis. Its antioxidant properties are also studied in models of oxidative stress. These studies provide valuable insights into the role of pyruvate in health and disease.

Absorption, Distribution and Excretion
Pyruvate is absorbed from the gastrointestinal tract and transported to the liver via the portal vein circulation. Metabolism/Metabolites In the liver, pyruvate is metabolized through multiple pathways.
The pharmacokinetic properties of pyruvic acid are characterized by its rapid absorption and metabolism. It is a small, water-soluble molecule that is readily taken up by cells and metabolized. It is a normal constituent of the body, and its levels are tightly regulated. It is metabolized primarily in the mitochondria via the pyruvate dehydrogenase complex and the citric acid cycle. Its half-life in the blood is very short, as it is rapidly cleared by tissues. For research purposes, pyruvic acid is typically stored at 2-8°C. It is a stable compound under normal storage conditions.

Toxicity Summary
Pyruvate can be converted into acetyl-CoA, serving as a biofuel. Acetyl-CoA enters the tricarboxylic acid cycle (Krebs cycle), where it is metabolized aerobically to produce ATP. Pyruvate can also be converted into lactate, providing energy under anaerobic conditions. Injection or perfusion of pyruvate enhances the contractile function of the heart during glucose or fatty acid metabolism. This positive inotropic effect is particularly pronounced in the heart due to ischemia/reperfusion injury. The positive inotropic effect of pyruvate requires intracoronary infusion. Its mechanism of action may include increased ATP production and enhanced ATP phosphorylation potential. Furthermore, pyruvate activates pyruvate dehydrogenase, promoting autooxidation by inhibiting pyruvate dehydrogenase kinase. Pyruvate dehydrogenase is inactivated in ischemic myocardium. Pyruvate's mechanism of action also includes reducing cytoplasmic inorganic phosphate concentration. As an antioxidant, pyruvate scavenges reactive oxygen species such as hydrogen peroxide and lipid peroxides. Indirectly, supraphysiological levels of pyruvate may increase intracellular levels of reduced glutathione.
The toxicological profile of pyruvic acid is well-established, as it is a normal metabolite. At physiological concentrations, it is non-toxic. However, at very high concentrations, it can cause metabolic acidosis and other adverse effects. It is a mild irritant to the skin, eyes, and respiratory tract. For laboratory handling, standard safety precautions should be observed, including the use of personal protective equipment (gloves, safety goggles, lab coat) and working in a well-ventilated area. It is intended for research use only and is not for human therapeutic or diagnostic use.

Pyruvate is a 2-keto monocarboxylic acid, a 2-keto derivative of propionic acid. It is a metabolite produced during glycolysis, an important metabolite and cofactor, functionally related to propionic acid, and is its conjugate acid. It is an intermediate product of carbohydrate, protein, and fat metabolism. In thiamine deficiency, its oxidation is inhibited, and it accumulates in tissues, especially in neural structures. (From Stedman, 26th edition) Pyruvate is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain). It has also been reported to be present in Cnidium monnieri, Drosophila melanogaster, and other organisms with relevant data. Pyruvate is an intermediate product of carbohydrate, protein, and fat metabolism. In thiamine deficiency, its oxidation is inhibited, and it accumulates in tissues, especially in neural structures. (From Stedman, 26th edition) Biological source: Intermediate product of primary metabolism (including fermentation processes). It exists in muscle and is in redox equilibrium with lactate. Pyruvate, a chiral cyclic acetal linked to sugar residues, is a common component of bacterial polysaccharides. It can be isolated from sugarcane fermentation broth and peppermint. It is also a component of Bauhinia, chickpea, flame tree, pea, and sweet clover. Uses/Importance: A reagent used to regenerate carbonyl compounds from aminourea, phenylhydrazone, and oxime. Pyruvate is a metabolite found or produced in Saccharomyces cerevisiae. It is an intermediate in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is inhibited, and it accumulates in tissues, especially in neural structures. (Excerpt from Stedman, 26th edition) Pharmacological Indications: Used for nutritional supplementation and also for treating dietary deficiencies or imbalances. Mechanism of Action: Pyruvate can be converted to acetyl-CoA, used as a biofuel. Acetyl-CoA enters the tricarboxylic acid cycle (Krebs cycle) and is metabolized under aerobic conditions to produce ATP. Pyruvate can also be converted to lactate, thus providing energy under anaerobic conditions. Injection or perfusion of pyruvate enhances the heart's contractile function during glucose or fatty acid metabolism. This positive inotropic effect is particularly pronounced in ischemic/reperfusion-injured hearts. The positive inotropic effect of pyruvate requires intracoronary infusion. Its mechanism of action may include increased ATP production and enhanced ATP phosphorylation. Another mechanism is the activation of pyruvate dehydrogenase, promoting autooxidation by inhibiting pyruvate dehydrogenase kinase. Pyruvate dehydrogenase is inactivated in ischemic myocardium. Furthermore, decreased cytoplasmic inorganic phosphate concentration is also a contributing factor to myocardial ischemia. As an antioxidant, pyruvate can scavenge reactive oxygen species such as hydrogen peroxide and lipid peroxides. Indirectly, supraphysiological levels of pyruvate may increase intracellular levels of reduced glutathione.
Pyruvic acid is the simplest alpha-keto acid. It is a key intermediate in glycolysis and the citric acid cycle. It is a colorless liquid with a pungent odor. It has a molecular formula of C₃H₄O₃ and a molecular weight of 88.06 g/mol. Pyruvic acid is also known as 2-oxopropanoic acid. It is a natural product and a secondary metabolite. It is for research use only.

C3H4O3

88.0621

88.016

127-17-3

1060

Colorless to light yellow <11°C solid powder,>12°C liquid

1.3±0.1 g/cm3

165.0±0.0 °C at 760 mmHg

13.8 °C

54.3±15.2 °C

1.0±0.6 mmHg at 25°C

1.417

-1.24

1

3

1

6

84

0

O([H])C(C(C([H])([H])[H])=O)=O

LCTONWCANYUPML-UHFFFAOYSA-N

InChI=1S/C3H4O3/c1-2(4)3(5)6/h1H3,(H,5,6)

2-oxopropanoic acid

2934.99.9001

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 (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~1135.59 mM)
DMSO : ≥ 50 mg/mL (~567.79 mM)

Solubility in Formulation 1: ≥ 2.63 mg/mL (29.87 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 26.3 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (28.39 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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (28.39 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.

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Solubility in Formulation 4: 100 mg/mL (1135.59 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)