Absorption, Distribution and Excretion
L-lactic acid is present in small amounts in the blood and muscle fluid of humans and animals; its concentration in these fluids increases after strenuous exercise. L-lactic acid is also present in the liver, kidneys, thymus, amniotic fluid, and other organs and fluids. A pre-infusion study in humans using radioactive L-lactic acid showed a virtual volume of distribution of 49.4% of body weight. The lactate pool size and turnover time were estimated to be 0.029 g/kg and 18.4 minutes, respectively. In vivo, lactate is distributed in proportion to or slightly less than the total body fluid volume. It diffuses readily across cell membranes, primarily via passive transport; under certain conditions, lactate distribution may be uneven, or the lactate pool may consist of several smaller pools with different rate constants. Transdermal absorption of a topical application of 5% [14C]-lactic acid (water-in-oil cream) was measured in rats. After 3 days, 50% of the applied lactate had penetrated the skin.
For more complete data on the absorption, distribution, and excretion of lactic acids (6 in total), please visit the HSDB record page.
Biodegradable nanoparticles (NPs) composed of polylactic acid (PLA) with an average particle size of 75 nm were prepared using a single emulsion method. When these particles were dripped into the vagina of estrous mice, they retrogradely crossed the cervix and reached the uterus. Uterine flushing following the injection of nanoparticles into the vagina showed that pro-inflammatory signals such as RANTES and TNF were induced in the uterus, which are detrimental to the establishment of pregnancy. These nanoparticles are being investigated for contraceptive purposes.
Rhodamine B (RhB)-labeled PLA nanoparticles were prepared by graft copolymerization of glycidyl methacrylate (GMA) onto PLA nanoparticles during an emulsion/evaporation process. RhB first binds to sodium dodecyl sulfate (SDS) via electrostatic interactions to form a hydrophobic complex (SDS-RhB). Due to the high affinity of SDS-RhB for GMA, the hydrophilic RhB can be successfully bound to PLA nanoparticles. The endocytosis of RhB-labeled PLA nanoparticles by macrophages was investigated using fluorescence microscopy. The effects of the surface properties and size of the PLA nanoparticles on endocytosis were studied. Results showed that PLA particles with a diameter less than 200 nm could avoid uptake by phagocytes. Compared to PLA particles surface-modified with polyethylene oxide-propylene oxide copolymer (F127) or polyvinyl alcohol (PVA), larger PLA particles (300 nm) surface-modified with polyethylene glycol (PEG) were endocytosed by macrophages to a lesser extent. Electrochemical impedance spectroscopy revealed the "stealth" effect of PEG on PLA nanoparticles, namely, its low protein adsorption, which allows them to avoid endocytosis by macrophages. Mucosal immunization aims to induce a strong immune response at the pathogen invasion portal. However, the fate mechanism of vaccine carriers co-administered with antigens remains incompletely elucidated, limiting further development of mucosal vaccines. Therefore, given the wide applicability of polylactic acid (PLA) nanoparticles as a vaccine carrier, we analyzed the fate of these PLA nanoparticles during in vivo and in vitro intestinal mucosal absorption to elucidate the mechanisms involved. We first designed specific fluorescent PLA nanoparticles that exhibited good colloidal stability after encapsulation with 6-coumarin or CellTrace BODIPY, and then monitored their transport in the mucosa in a mouse ileal ligation model. The transport process of the particles appeared to follow a three-step process. Most particles were first captured by mucus. Then, they crossed the epithelial barrier only through M cells, eventually accumulating in Peyer's lymphoid aggregates (PP). Finally, we observed specific interactions between these PLA nanoparticles and B cells and dendritic cells (DCs) in the PP. Furthermore, we demonstrated that dendritic cells (DCs) that engulfed certain nanoparticles exhibited TLR8+-specific expression. This specific targeting of these two cell types strongly supports the use of PLA nanoparticles as an oral vaccine delivery system. In fact, we observed the same biodistribution pattern after oral administration of PLA nanoparticles to mice, indicating that these nanoparticles can specifically reach the immune targets required for oral immunization.

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Metabolism/Metabolites
...Propylene glycol... is oxidized to lactate or pyruvate via two pathways. These two metabolites are then used by the body as energy sources, one through oxidation via the tricarboxylic acid cycle and the other through glycolysis to generate glycogen.
Lactic acid diffuses through muscle tissue and is transported to the liver via the bloodstream. In the liver, it is converted to glucose via gluconeogenesis. Lactic acid can also be further metabolized in the lactate cycle (also known as the Corrie cycle).
L-lactic acid is a normal metabolic intermediate produced by most mammalian cells and other organisms (such as bacteria); in humans, dogs, and rats, L-lactic acid is metabolized preferentially over D-lactic acid. Lactic acid is converted to pyruvate by lactate dehydrogenase.
In animals, lactate produced by anaerobic metabolism can be transported to other aerobic tissues, such as the liver, where it can be reconstituted into pyruvate. Pyruvate can then be further metabolized, reverting to carbohydrates such as free glucose, or stored as glycogen. For more complete data on the metabolism/metabolites of lactic acid (a total of 8 metabolites), please visit the HSDB record page. In August 2004, the U.S. Food and Drug Administration (FDA) approved an injectable medical device based on poly-L-lactic acid (PLLA) for the restoration and/or correction of facial fat loss (lipatrophy) in individuals infected with the human immunodeficiency virus. Therefore, the properties of PLLA microparticles have attracted widespread attention in the medical community. Polylactic acid has a long history of safe use in medical applications, such as as nails, plates, screws, intraosseous and soft tissue implants, and as a carrier for the sustained release of bioactive compounds. The L-isomer of polylactic acid is a biodegradable, biocompatible, and bioinert synthetic polymer. It is speculated that the presence of PLLA microparticles will induce a normal foreign body reaction, thereby initiating collagen regeneration. Over time, collagen buildup creates volume at the injection site, while PLLA microparticles are metabolized into carbon dioxide and water and expelled through the respiratory system. /Poly-L-Lactic Acid/
Polylactic acid (PLA) was introduced in 1966 for use in biodegradable surgical implants. The hydrolysis product is lactic acid, a normal intermediate in carbohydrate metabolism. Polyglycolic acid sutures exhibit a predictable degradation rate consistent with the healing process of natural tissues.

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Biological Half-Life
(32)P-chromium phosphate-poly-L-lactic acid ((32)P-CP-PLLA) has a mean effective half-life of 11.8 days.

Toxicity Summary
Identification and Uses: Lactic acid forms yellow to colorless crystals or a 50% syrupy liquid. It has wide applications in dyeing baths, serving as a mordant for wool products and a solvent for water-insoluble dyes. It is also used to reduce chromates in wool mordant production and in cheese and confectionery production. Lactic acid is an ingredient in infant formula; an acidifier in beverages; and is also used for acidifying brewing wort. It is used in the preparation of sodium lactate injections, as well as as an ingredient in cosmetics and spermicidal gels. Other uses: For the removal of Clostridium butyricum in yeast production; for depilating, enriching, and decalcifying leather; as a solvent for cellulose formate; and as a flux in soft solders. Lactic acid is used to produce lactates, which are used in food, pharmaceuticals, and as solvents. It is also a plasticizer and a catalyst in phenolic resin casting. Human Exposure and Toxicity: Its effects on the eyes are similar to other moderately strong acids, causing initial coagulation of the corneal and conjunctival epithelium, but with good prognosis if rinsed promptly with water. In humans, accidental intraduodenal administration of 100 ml of 33% lactate solution can be fatal within 12 hours. Hyperlactatemia and lactic acidosis are among the most dangerous and life-threatening side effects during treatment with certain nucleoside reverse transcriptase inhibitors. Lactic acidosis is associated with both hereditary and acquired metabolic disorders. Abnormal lactate metabolism is a major factor in many diseases, particularly in cases of gluconeogenesis, anaerobic glycolysis, and acid-base imbalances. Lactic acid can only be produced from pyruvate; therefore, diseases that increase pyruvate concentration, enhance lactate production, or reduce lactate degradation can lead to lactic acidosis. Congenital metabolic defects accompanied by disturbances in glucose, pyruvate, amino acid, and organic acid metabolic pathways, as well as toxic and systemic diseases that promote tissue hypoxia or mitochondrial damage, can all lead to lactic acidosis. Animal experiments: Lactic acid was instilled into the eyes of rabbits using standard methods; the reaction score after 24 hours was 8 points (out of 1-10). Prolonged contact of lactic acid solutions (both undiluted and 50% aqueous solutions) with rabbit eyes can lead to corneal necrosis and persistent stromal scarring. Male rats were divided into several groups of five, each receiving 0.5 mL of lactic acid solution at concentrations of 130, 650, or 1300 mg/2000 kg body weight via gastric tube; the control group received an equal volume of physiological saline. Two rats in the 650 mg group and one rat in the 1300 mg group died within 24 hours of administration. Eight days later, the rats were given the same dose of lactic acid. Two rats in the 1300 mg group died; these animals immediately exhibited symptoms such as dyspnea, rhinorrhea, vomiting, and abdominal distension after administration. Adding approximately 3.6–18 g/kg lactic acid to feed or drinking water and feeding pigs continuously for up to 5 months did not result in significant toxic reactions. Drunken sheep syndrome has been described as lamb D-lactate acidosis syndrome. In a developmental study, 12 mice were administered 570 mg/kg lactate daily by gavage from days 6 to 15 of gestation; 13 mice served as a control group and were given distilled water. All female mice were sacrificed on day 18 of gestation. There was no significant difference in gestational weight gain between the experimental and control groups, but the feed intake in the experimental group was significantly lower than that in the control group. Furthermore, the relative liver weight of the female mice in the experimental group was also significantly lower than that in the control group. The only observed effect on the fetus was a statistically significant increase in delayed parietal bone ossification. Female rabbits were administered 0.1–0.2 g/kg lactate (dissolved in 100–150 mL of water) orally twice daily for 5 months; another 5 female rabbits were administered 0.1–0.7 g/kg lactate (dissolved in 50–100 mL of water) orally twice daily for 16 months (actual treatment lasted 13 months). No tumors were reported at either 5 or 16 months. Mutagenicity of 90.5% pure lactate in phosphate buffered saline was tested using metabolically activated Salmonella Typhimurium strains TA92, TA1535, TA100, TA1537, TA94, and TA98 via the Ames test, and all results were negative. Without metabolic activation, the Ames test was performed on 1000 μg/mL, 11 mM lactate using a clonal subline of Chinese hamster lung tissue, and the results were negative. The detection of chromosomal aberrations by lactate was also negative. Ecotoxicity studies: Studies have shown that feeding 10% lactate to a diet rich in carbohydrates, protein, or fat can lead to polyneuritis crises in birds similar to vitamin B1 deficiency. Identification and uses: Polylactic acid (PLA) is a bioabsorbable polymer. It is used in industrial packaging and in the biocompatible/bioabsorbable medical device market. PLA was first approved in Europe in 1999 for use as a soft tissue filler to improve the cosmetic appearance of scars and wrinkles. In the United States, it is used to repair and/or correct symptoms of facial fat loss (lipomatosis) in HIV-infected individuals. Human Exposure and Toxicity: In August 2004, the U.S. Food and Drug Administration (FDA) approved an injectable medical device based on polylactic acid (PLA) for repairing and/or correcting symptoms of facial fat loss (lipomatosis) in HIV-infected individuals. Therefore, the properties of PLA microparticles have attracted widespread attention in the medical community. Polylactic acid has a long history of safe use in medical applications, such as as nails, plates, screws, intraosseous and soft tissue implants, and as a carrier for the sustained release of bioactive compounds. The L-isomer of polylactic acid is a biodegradable, biocompatible, and bioinert synthetic polymer. It is speculated that the presence of PLA microparticles will trigger a normal foreign body reaction, thereby initiating collagen regeneration. Over time, collagen buildup creates volume at the injection site, while PLA microparticles are metabolized into carbon dioxide and water and expelled through the respiratory system. Adverse reactions have been observed after injection of poly-L-lactic acid (PLA), primarily including hematoma, ecchymosis, edema, discomfort, inflammation, and erythema. The most common adverse reaction to PLA is delayed onset of subcutaneous papules, which are localized to the injection site, usually palpable, asymptomatic, and invisible. Post-marketing observed adverse reactions include: central nervous system—fatigue, poor efficacy, discomfort; skin—application site discharge, ectropion, skin hypertrophy, injection site abscess, injection site atrophy, injection site lipoma, injection site granuloma, injection site reaction, rash, rough skin, telangiectasia, and visible nodules (with or without inflammation or abnormal pigmentation). Other adverse reactions include: arthralgia, allergic reactions, angioedema, nail brittleness, colitis (not otherwise specified), hair breakage, hypersensitivity reactions, photosensitivity reactions, and angioedema. Animal Studies: In rat studies, PLA exhibited good biocompatibility, and the studied tissues tolerated it well, with no chromosomal mutagenicity observed. The effects of different molecular weights of polylactic acid (PLA) on cell proliferation were investigated using rat epithelial cells under in vitro culture conditions. Overall, PLA demonstrated satisfactory biocompatibility, but some cell inhibition was observed. In some early animal studies, PLA induced symptoms associated with chronic inflammation (presence of macrophages, fibroblasts, giant cells, and lymphocytes). These inflammatory changes were independent of bacterial infection.

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Toxicity Data
LC50 (rat) = 7,940 mg/m3/4hr

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Interactions
This study investigated the effects of local myocardial administration of lactic acid in combination with low-dose edaravone to determine whether this combination provided benefits similar to mechanical posttreatment.
We randomly assigned 108 rats to six groups: sham operation, reperfusion injury, posttreatment, lactate (Lac), low-dose edaravone (Eda), and lactate + low-dose edaravone (Lac+Eda). Before administration, the left coronary artery of the rats was occluded for 45 minutes. Rats were sacrificed at different time points to detect infarct area, serum markers of myocardial injury and apoptosis, and the expression of signaling pathway markers. We found that the infarct area induced by ischemia-reperfusion injury was significantly reduced after posttreatment and lactate + edaravone injection; similar trends were observed in serum myocardial injury markers, apoptosis markers, and hemodynamic parameters. Compared with the posttreatment group, the lactate + edaravone group showed similar levels of blood pH, reactive oxygen species (ROS), mitochondrial uptake, and signaling pathway markers. The lactate and edaravone groups partially mimicked this protective effect. These data suggest that local myocardial injection of lactate and low-dose edaravone can initiate the protective signaling pathways of mechanical posttreatment and replicate the cardioprotective effect.
Mosquitoes use carbon dioxide and L-lactic acid, exhaled and exhaled, to provide olfactory signals that enable them to locate and bite humans; however, different mosquito species exhibit variations in this regard. This study investigated the upwind response of Anopheles skeletalii (Mysore type), an important malaria vector in Asia, to carbon dioxide and L-lactic acid under laboratory conditions. Results showed that the lowest dose of carbon dioxide (90 ppm) activated mosquitoes, while ten times the dose inhibited their activity. L-lactic acid alone did not produce a significant effect, but mosquitoes were attracted when added to carbon dioxide solutions ranging from 90 to 410 ppm at a rate of 6 μg/min. These results further support the hypothesis that carbon dioxide plays an important role in the host-finding behavior of zoophilic mosquitoes and suggest that L-lactic acid may be more critical than carbon dioxide in attracting Anopheles skeletalii.
During the pulmonary edema phase… metabolic acidosis may occur due to increased lactate production caused by hypoxemia. /NO2-Induced Acute Lung Injury/
Burning and/or stinging sensations are among the most frequently reported problems by patients using topical therapies for skin conditions. Topical lactic acid preparations are commonly used to treat dry, flaky skin. This study compared the degree of burning/sting reported by subjects after using 10% lactic acid cream, 12% ammonium lactate emulsion, and cetearyl alcohol emulsion containing strontium. The mean burning/sting scores of the 10% lactic acid cream and cetearyl alcohol emulsion were lower than those of the 12% ammonium lactate emulsion (P<0.0001). Based on the results, the 10% lactic acid cream containing strontium caused less burning/sting than the 12% ammonium lactate emulsion.
For more (complete) data on interactions of lactic acids (6 in total), please visit the HSDB record page.
The development of a novel environmentally friendly antimicrobial packaging involves coating a polylactic acid (PLA) film surface with arginine lauryl ester (LAE) after corona discharge activation. Analysis using scanning electron microscopy (SEM) confirmed the successful coating of LAE onto the PLA surface. The mechanical properties of LAE/PLA films with different LAE coating amounts (0% to 2.6% [w/w]) were essentially the same as those of pure PLA films. Antimicrobial activity against Listeria monocytogenes and Salmonella typhimurium was confirmed by a modified agar diffusion qualitative test and the JIS Z 2801:2000 quantitative method. Using LAE/PLA film as a food contact antimicrobial packaging model system for cooked cured ham, the results showed that coating PLA with a 0.07% (w/w) LAE coating effectively inhibited Listeria monocytogenes and Salmonella typhimurium on ham when high transparency was required. This was confirmed by a 2 to 3 log-unit reduction in pathogen growth on each film layer after 7 days of storage. However, when the LAE coating content reaches 2.6% (w/w), the antibacterial activity is stronger, but the transparency of the finished product is reduced. This article demonstrates how to use corona discharge to coat the surface of polylactic acid (PLA) with a laser-assisted corona discharge (LAE) coating, thereby easily developing functional green food packaging with highly efficient antibacterial activity. Practical application: This article verifies the effectiveness of an innovative antibacterial LAE-coated PLA film against foodborne pathogens. Importantly, the preparation of the LAE-coated PLA film can be customized on existing film production lines.
Injectable products are gaining popularity as an alternative to surgery for reversing signs of facial aging. In 2012, nearly 5 million injectable treatments were performed in the United States. Due to their complementary mechanisms of action, volume-filling products such as hyaluronic acid (HA), calcium hydroxyapatite (CaHA), and poly-L-lactic acid (PLLA) are often used in combination with other products and neurotoxins for facial rejuvenation. This article presents two case reports involving patient-specific combinations of two different hyaluronic acid (HA) products (injectable poly-L-lactic acid (PLLA) and calcified hyaluronic acid (CaHA)) with botulinum toxin type A (incobotulinumtoxin A or abobotulinumtoxin A). The combined use of HA, CaHA, PLLA, and neurotoxins has yielded significant therapeutic effects in many patients, and no clinical evidence has been found that the combination therapy increases adverse events. /Poly-L-lactic acid/
Degradable polymer-based materials are attractive in orthopedics and dentistry as alternatives to metal implants for bone fixation. This article combines the degradable polymer polylactic acid (PLA) with novel carbon nanotube (CNT)-calcium phosphate (CP) hybrid nanopowders for this application. Specifically, we prepared CNTs-CP hybrid nanopowders (CNT contents of 0.1% and 0.25%, respectively) using ion-modified carbon nanotube (mCNT) solutions. The mCNTs solution, specially synthesized, exhibits excellent dispersibility and can effectively adsorb onto CP nanoparticles. Subsequently, we mixed the mCNTs-CP hybrid nanoparticles with PLA (up to 50%) to prepare mCNTs-CP-PLA nanocomposites. The addition of mCNTs-CP hybrid nanoparticles significantly improved the mechanical tensile strength of the nanocomposites. Furthermore, the nanocomposites with low concentrations of mCNTs (0.1%) showed significant biological effects on gene and protein expression, including cell proliferation and osteoblast differentiation. Based on this study, adding novel mCNT-CP hybrid nanoparticles to PLA biopolymers can be considered a novel material option for developing hard tissue implants. Temporary cardiovascular stent devices made from bioabsorbable materials may reduce late stent thrombosis. A water-soluble amphiphilic phospholipid polymer (PMB30W) containing phosphorylcholine groups was mixed with high molecular weight polylactic acid (PLLA) to reduce adverse tissue reactions on the surface. PLLA implants and polymer hybrid implants (PLLA/PMB30W) were implanted subcutaneously in rats, in the rat subrenal abdominal aorta, and in the rabbit internal carotid artery, respectively. Six months after subcutaneous implantation, the PLLA/PMB30W surface maintained a high density of phosphorylcholine groups, with no significant bioresorption. Histomorphometry was performed on the cross-sectional area of polymer tubes with a diameter less than 1.6 mm after intravascular implantation. Compared to PLLA tubes, PLLA/PMB30W tubes significantly reduced thrombus formation within 30 days of implantation. Human peripheral blood mononuclear cells were cultured on PLLA and PLLA/PMB30W tubes to compare inflammatory responses. Enzyme-linked immunosorbent assay (ELISA) quantitative analysis showed significantly reduced levels of pro-inflammatory cytokines in the PLLA/PMB30W group, which were almost identical to those in the negative control group. Therefore, we conclude that phosphorylcholine groups can significantly reduce tissue responses in vivo and in vitro, and PLLA/PMB30W is a promising material for the fabrication of temporary cardiovascular stent devices.

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Non-human toxicity values
Rats oral LD50: 3730 mg/kg
Guinea pig oral LD50: 1810 mg/kg
Mice subcutaneous injection LD50: 4500 mg/kg
Mice oral LD50: 4875 mg/kg
Rats inhalation LC50: 7.94 mg/L/4 hr

Lactic acid is a colorless to pale yellow, odorless, viscous liquid that is corrosive to metals and tissues. It is used in the production of fermented dairy products, as a food preservative, and in the manufacture of chemicals. 2-Hydroxypropionic acid is a 2-hydroxy monocarboxylic acid, a product of propionic acid where one α-hydrogen is replaced by a hydroxyl group. It is a metabolite of Daphnia magna and algae, functionally related to propionic acid, and is the conjugate acid of lactic acid. It is a normal intermediate in sugar fermentation (oxidation, metabolism). Concentrated forms are used for oral administration to prevent gastrointestinal fermentation. (From Stedman, 26th edition) Sodium lactate is the sodium salt of lactic acid and has a slightly salty taste. Lactic acid is produced by fermenting sugar sources (such as corn or beets) and then neutralizing the lactic acid produced, yielding a compound with the molecular formula NaC3H5O3. Lactic acid is one of the active ingredients in Phexxi, a non-hormonal contraceptive approved by the FDA in May 2020.
It has been reported that lactic acid is found in fruit flies, elderberries, and several other organisms with relevant data.
DL-lactic acid is a racemic isomer of lactic acid, which is a biologically active isomer in the human body. Lactic acid or lactate is produced during the fermentation of pyruvate by lactate dehydrogenase. This reaction produces lactic acid and nicotinamide adenine dinucleotide (NAD), which is then used in glycolysis to generate adenosine triphosphate (ATP), an energy source.
It is a normal intermediate product in the process of sugar fermentation (oxidation, metabolism). The concentrated form is used orally to prevent gastrointestinal fermentation. (Excerpt from Stedman, 26th edition)
Drug Indications

Used as an alkalizing agent.
Mechanism of Action

Lactate ions are ultimately metabolized into carbon dioxide and water, a process that requires the consumption of hydrogen ions.

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Therapeutic Use
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that lists human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov provides summary information on the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the study title, description, and design; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). The database contains lactic acid.
(Veterinary): Formerly used as a corrosive agent, diluted for rinsing tissues; used as an intestinal antiseptic and anti-fermentation agent.
A 10% solution is used as a bactericide for neonatal skin. ...A 16.7% solution dissolved in flexible collodion is used to remove warts and small skin tumors.
Acidifying agent
Sustained-release formulation; artificial membrane; dental implant; drug delivery system
Used to restore and/or correct symptoms of facial fat loss (lipomatosis) in individuals infected with HIV.
Exploratory treatment We report a case of facial volume restoration using injectable poly-L-lactic acid (PLLA) for a 45-year-old white woman who was concerned about the appearance of her hands. The patient desired long-term improvement and chose injectable PLLA because of its known efficacy lasting up to 2 years, although she was informed that injectable PLLA was not yet FDA approved for use on the hands. After mixing injectable PLLA with 8 mL of diluent and lidocaine, 0.1–0.2 mL aliquots were injected into selected sites, with a maximum of 5 mL per hand. The patient received the same treatment three times, followed by the application of a moisturizing cream and massage; the patient noticed an improvement in appearance between the second and third treatments. The corrective effect lasted for at least 18 months without any adverse events. We also briefly reviewed the literature on injectable poly-L-lactic acid (PLLA) for hand volume restoration. /Poly-L-lactic acid/
Characteristics of facial aging include soft tissue atrophy, loss of skin elasticity leading to facial skin laxity, and sagging of facial soft tissue or ptosis due to gravity. Poly-L-lactic acid (PLLA) is a synthetic, biodegradable polymer that fills soft tissue by stimulating an inflammatory tissue response and subsequently promoting collagen deposition. This paper discusses the specificities of facial aging, describes the mechanism of action and indications of a novel PLLA filler undergoing FDA approval… and details the results of a two-year off-label pilot study of the product. During the FDA-approved pilot study for cosmetic use, 106 patients received off-label treatment with PLLA. All patients were followed up for two years to help develop injection technique protocols. The patients in this series of studies ranged in age from 40 to 78 years. There were 3 men and 103 women. Patients received an average of 1.6 vials per treatment, with an average of 2.3 treatment sessions, to achieve volume filling in the tear troughs, midface, cheekbones, nasolabial folds, premandibular region, mandibular border, and mandibular angle. The study achieved a 100% follow-up rate and a patient satisfaction rate of 99.1%. The nodule formation rate was 4.7% during the at least two-year follow-up period. Due to its unique mechanism of action, polylactic acid (PLLA) for non-surgical facial rejuvenation requires precise injection techniques, with particular attention to optimizing treatment outcomes and minimizing adverse reactions. Poly-L-lactic acid. For more complete data on the therapeutic uses of poly-L-lactic acid (17 types), please visit the HSDB record page.

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Drug Warnings
For patients with active skin inflammation or infection in or near the treatment area, the use of poly-L-lactic acid should be postponed until the inflammation or infection is controlled. Poly-L-lactic acid should be injected into the deep dermis or subcutaneous tissue. Avoid superficial injections. Extra caution should be exercised when using poly-L-lactic acid in areas with thinner skin. The safety and efficacy of poly-L-lactic acid in the periocular area have not been established. Do not overcorrect (overfill) contour defects, as depressions will gradually improve over several weeks as the effects of poly-L-lactic acid treatment become apparent. /Poly-L-lactic acid/ For more complete data on drug warnings for polylactic acid (16 in total), please visit the HSDB record page.

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Pharmacodynamics
Lactic acid produces a metabolic alkalizing effect.

(C3H6O3)X

60000(Average)

90.031

26100-51-6

26100-51-6

612

Crystals (melt at 16.8 °C)
Yellow to colorless crystals or syrupy 50% liquid
Viscous, colorless to yellow liquid or colorless to yellow crystals
Glassy material
High-molecular-weight poly(lactic acid) is a colorless, glossy, stiff thermoplastic polymer

1.25-1.28 g/cm3

227.6±0.0 °C at 760 mmHg

176 ºC

109.9±16.3 °C

0.0±1.0 mmHg at 25°C

1.451

-0.7

2

3

1

6

59.1

0

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

JVTAAEKCZFNVCJ-UHFFFAOYSA-N

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

2-hydroxypropanoic 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)

DMSO: 250 mg/mL

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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