L-Lactic acid is an agonist of the hydroxycarboxylic acid receptor 1 (HCA1, also known as HCAR1). It is a natural ligand for this receptor, which is involved in metabolic regulation. It also serves as a substrate for lactate dehydrogenase (LDH) and lactate oxidase.

L-Lactic acid activates the HCA1 receptor, which is a G protein-coupled receptor. It has been shown to significantly inhibit LPS-induced cytokine induction in mice following endotoxemia. L-Lactic acid treatment decreased glucose uptake and lactate output during LPS stimulation.

In mice, L-Lactic acid significantly inhibited LPS-induced cytokine induction following endotoxemia. It decreased glucose uptake and lactate output during LPS stimulation. These findings indicate that L-Lactic acid has immunomodulatory effects in vivo, dampening the inflammatory response.

The in vitro assay for HCA1 receptor activation involves measuring the receptor's activity in response to L-Lactic acid. Cells expressing HCA1 are treated with L-Lactic acid, and downstream signaling (such as calcium flux or cAMP levels) is measured. The EC50 for receptor activation is determined from the dose-response curve.

Specific in vitro cell-based assay protocols for L-Lactic acid are not detailed. However, its activity can be assessed in immune cells, such as macrophages, by measuring the production of cytokines (e.g., TNF-α, IL-6) in response to LPS stimulation in the presence or absence of L-Lactic acid. This assay would evaluate its immunomodulatory effects.

In the mouse model of endotoxemia, L-Lactic acid was administered to mice prior to LPS challenge. Cytokine levels in the blood were measured to assess the anti-inflammatory effect. This is a standard model for studying the immunomodulatory effects of compounds.

L-Lactic acid is an endogenous metabolite that is rapidly cleared from the body. Its plasma concentration is tightly regulated and increases during conditions of tissue hypoxia or intense exercise. It is transported across cell membranes by monocarboxylate transporters (MCTs) and is metabolized primarily in the liver.

Toxicity Summary
The accumulation of L-lactic acid in the body has been proven toxic. In lactic acidosis, excess intracellular lactate is released into the bloodstream, and cations are also released to maintain blood electroneutrality. This lowers blood pH. Lactic acid may exert a strong effect on the GABAergic network of the developing brain, making its inhibitory effect stronger than previously thought, possibly through better support of metabolites, alteration of intracellular basal pH, or both. (Wikipedia) Toxicity Data
LC50 (Rats) > 7,940 mg/m³/4hr
Accumulation of L-Lactic acid in the body can be toxic, leading to lactic acidosis. This condition is characterized by low blood pH and can occur in various pathological states, including sepsis, shock, and hypoxia. However, at physiological concentrations, L-Lactic acid is an important metabolic intermediate.

(S)-Lactate is the optical isomer of lactate with the (S)-configuration. It is a metabolite in both E. coli and humans. It is a 2-hydroxypropionic acid and also a (2S)-2-hydroxy monocarboxylic acid. It is the conjugate acid of (S)-lactate and the enantiomer of (R)-lactate. L-Lactate is a metabolite found or produced in E. coli (strains K12 and MG1655). L-Lactate has also been reported in Arabidopsis thaliana, humans, and other organisms with relevant data. L-Lactate is the levorotatory isomer of lactate and is a biologically active isoenzyme in humans. Lactate or lactate salt is produced during the fermentation of pyruvate by lactate dehydrogenase. In addition to producing lactate, this reaction also produces nicotinamide adenine dinucleotide (NAD), which is subsequently used in glycolysis to generate adenosine triphosphate (ATP), an energy source. Lactate is involved in a variety of biochemical processes and is produced in muscles during strenuous exercise. Traditionally, lactate levels in critically ill patients have been used to stratify patients with poor prognoses. However, plasma lactate levels are the result of a delicate interplay of multiple factors that influence the balance between lactate production and clearance. When oxygen supply and consumption are mismatched, organisms like humans, forced to produce ATP to sustain themselves, adapt in various ways until energy exhaustion occurs. Lactate, as part of the adaptive response, can be used to assess the severity of the supply-demand imbalance. In this context, the timing of intervention is crucial: early and effective treatment can restore cells to a normal state as long as the oxygen supply mechanisms (i.e., mitochondria) remain intact. Conversely, once mitochondrial dysfunction occurs, energy exhaustion can occur even under normal oxygenation conditions. Therefore, elevated lactate levels in critically ill patients can be seen as an early marker of a potentially reversible state. Multiple studies have shown that malignant transformation is associated with increased glycolytic flux and increased lactate excretion from anaerobic and aerobic cells. At initial diagnosis, quantitative bioluminescence imaging was used to examine various primary cancers (cervical cancer, head and neck cancer, colorectal cancer) in patients. It was found that lactate concentrations in different tumors or within the same lesion could be relatively low or extremely high (up to 40 μmol/g). In all tumor types studied, high lactate concentrations were associated with a higher incidence of distant metastasis in the early stages of the disease. Low-lactate tumors (median approximately 8 μmol/g). Lactate dehydrogenase expression was upregulated in most of these tumors compared to surrounding normal tissue (A3333, A3334). L-lactic acid is a metabolite found or produced in Saccharomyces cerevisiae. It is a normal intermediate in the process of sugar fermentation (oxidation, metabolism). Concentrated forms are used for oral administration to prevent gastrointestinal fermentation. (From Stedman, 26th edition)
See also: Polylactic acid, L- (monomer); Arnica; Lactic acid, L-; Zinc oxide (component); Lactic acid (note moved to)...See more...

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Drug indications
Contraception
L-Lactic acid is a key metabolite involved in cellular metabolism and energy production. It serves as a substrate for gluconeogenesis and is a signaling molecule through its action on HCA1. It is also a biomarker for tissue hypoxia and is used in the production of biodegradable plastics. It is not a drug but has diagnostic and industrial applications.

C3H6O3

90.07

90.031

79-33-4

Sodium (S)-2-hydroxypropanoate;867-56-1;L-Lactic acid-13C3;87684-87-5;L-Lactic acid-2-13C1;740788-63-0

107689

Colorless to light yellow <53°C powder,>53°C liquid

1.3±0.1 g/cm3

227.6±0.0 °C at 760 mmHg

52-54°C

109.9±16.3 °C

0.0±1.0 mmHg at 25°C

1.451

-0.7

2

3

1

6

59.1

1

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

JVTAAEKCZFNVCJ-REOHCLBHSA-N

InChI=1S/C3H6O3/c1-2(4)3(5)6/h2,4H,1H3,(H,5,6)/t2-/m0/s1

(2S)-2-hydroxypropanoic acid

L-(+)-Lactic acid; Paralactic acid; L-Lactic 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, 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 (~1110.12 mM)
DMSO : ~100 mg/mL (~1110.12 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (23.09 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 20.8 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: ≥ 2.08 mg/mL (23.09 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 20.8 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: ≥ 2.08 mg/mL (23.09 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 20.8 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 (1110.12 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.)