Ingredientsα-Ketoglutaric acid (AKG) is an organic compound with the formula HO₂CCO(CH₂)₂CO₂H. A white, nontoxic solid and a common dicarboxylic acid, it exists in water as its conjugate base, α-ketoglutarate. It is also classified as a 2-ketocarboxylic acid. The compound is widely referred to by several systematic and common names: alpha-ketoglutaric acid (also known as 2-oxo-glutaric acid, 2-oxopentanedioic acid) has been found in all living organisms and is an important cellular low-molecular-mass metabolite. "Ketoglutaric acid" and "ketoglutarate," when not qualified as α or β, almost always refer respectively to α-ketoglutaric acid or α-ketoglutarate.
α-Keto acids have the keto group adjacent to the carboxylic acid and play a central role in cell metabolism, including pyruvic acid, oxaloacetic acid, and α-ketoglutarate. Since the stability of the carboxyl group is affected by its interaction with the carbonyl group in α-keto acids, free α-keto acids are unstable and rarely detected in nature.
Oxidative decarboxylation of isocitrate in the TCA cycle and oxidative desamination of glutamate are the main sources of AKG in the cell. The body can also produce AKG when metabolizing amino acids, particularly glutamate. Animal items like meat, fish, and dairy are natural sources of AKG. AKG can also be obtained from natural sources such as fruits and vegetables; grapes are a particularly rich source of AKG.
AKG levels in the body decline significantly with age — studies show that the concentration at age 80 is only about 10% of the value present at age 40. This age-related decline has sparked scientific interest in AKG as a potential agent for influencing age-related processes.
Alpha-ketoglutarate may be combined with other substances, including amino acids and minerals, to form "combination ingredients." Some common examples include L-arginine alpha-ketoglutarate (AAKG), ornithine ketoglutarate (OKG), and calcium alpha-ketoglutarate (Ca-AKG). These combination ingredients are intended to increase the levels of both substances in the body, and each of these substances can cause different effects and side effects.
The calcium form (Ca-AKG) was developed to improve the bioavailability and stability of AKG, making it particularly interesting for therapeutic applications. Ornithine alpha-ketoglutarate (OKG) is a salt composed of one molecule of ketoglutarate and two of ornithine.
Today, AKG is synthesised chemically, but attempts have been made at biotechnological production of this metabolite by various bacteria and yeast. AKG can be produced through the fermentation of specific bacteria strains, such as Bacillus subtilis and Corynebacterium glutamicum, which convert glutamate to AKG.
Alpha-ketoglutarate is an endogenous metabolite rather than a plant-derived botanical; therefore, it does not carry a traditional ethnobotanical or folk medicine history of the kind found for herbal ingredients. Unlike plant-based supplements, AKG was not formally identified or isolated until the elucidation of the Krebs (citric acid) cycle in the mid-20th century. Since the discovery and description of the Krebs cycle, a number of features and functions of AKG have been identified. Yet, many of the AKG actions are still waiting to be discovered. However, current knowledge about this metabolite already ensures its practical application in various fields of human life.
The earliest clinical use of AKG emerged in the context of parenteral and enteral nutrition — particularly for surgical patients. A few studies published in the 1980s and 1990s in humans suggested the potential benefits of AKG in muscle growth, wound healing, and in promoting faster recovery after surgery. WO 89/03688 discloses that alpha-ketoglutarate has the same effect as glutamine when given to postoperative patients; preliminary tests on patients subjected to a biliary tract operation showed that an addition of alpha-ketoglutarate to a conventional parenteral nutritional support program improves the nitrogen balance of the patients.
Initial clinical studies on AKG were conducted in patients with specific health conditions, such as encephalopathy, stroke, chronic renal failure, or in bedridden individuals. However, research on AKG supplementation in healthy populations remains limited. Ornithine alpha-ketoglutarate (OKG) has a longer clinical history, particularly in European hospital settings. OKG is a natural compound derived from the amino acids ornithine and glutamine, which are classified as conditionally essential, meaning that while the body typically produces them, additional supplementation may be necessary during periods of severe stress, such as recovery from significant injuries, major surgeries, or severe illnesses.
α-Ketoglutarate is an intermediate in the citric acid cycle, a set of cyclic reactions that supplies energy to cells. It is also an intermediate in or product of several other metabolic pathways. These include pathways that make amino acids and in the process regulate the cellular levels of carbon, nitrogen, and ammonia; reduce the cellular levels of potentially toxic reactive oxygen species; and synthesize the neurotransmitter γ-aminobutyric acid (GABA).
α-KG is crucial for the coordination of carbon and nitrogen due to its role as a critical intermediate in the TCA cycle and amino acid metabolism. α-KG is also closely related to proteins, lipids, vitamin synthesis, and energy metabolism.
NH₄⁺ is coupled to alpha-ketoglutarate (AKG), a reaction which results in the appearance of glutamate, and after that, in the appearance of glutamine. The surplus of NH₄⁺ which is not utilized by AKG/glutamate/glutamine is eliminated as urea in the urine, via the urea cycle in hepatocytes. Alpha-ketoglutarate is a precursor of glutamine which contributes to muscle repair, prevents protein catabolism, improves nitrogen retention, functions as an immunomodulatory molecule, and takes part in proper function of the intestines.
Alpha-ketoglutarate (αKG) is a known potential highly antioxidative agent for radical oxidative species such as peroxides. AKG is also involved in antioxidative processes. It scavenges reactive oxygen species (ROS) and reactive nitrogen species and supports the activity of endogenous antioxidant enzymes (superoxide dismutase (SOD) and catalase), thereby protecting cells from oxidative stress.
AKG is an obligatory co-substrate for 2-oxoglutarate-dependent dioxygenases, which catalyse hydroxylation reactions on various types of substrates. In humans, there are more than 60 different 2-OGDDs, and some of these enzymes play a key role in physiologically important processes such as the hypoxic response, fatty acid metabolism, nucleic acid repair and modification, and epigenetic regulation.
AKG regulates the activity of prolyl-4 hydroxylase, which controls the biosynthesis of collagen, a component of bone tissue. Alpha-ketoglutarate is a precursor of glutamate, which may be converted to proline, an important component of collagen. Alpha-ketoglutarate also participates in the conversion of proline to 4-hydroxyproline. The proline residues in collagen may be hydroxylated at C-4 by prolyl hydroxylase to form 4-hydroxyproline, for which alpha-ketoglutarate, molecular oxygen, and ascorbate are required.
AKG regulates the activity of the Jumonji C domain-containing lysine demethylases (KDM2–7) and ten–eleven translocation hydroxylases (TET1–3), i.e., enzymes involved in histone and DNA demethylation, respectively. Although primarily generated in mitochondria through the TCA cycle, AKG is transported to the cytosol and nucleus, where it supports the activity of TET DNA demethylases and Jumonji C domain-containing histone demethylases. In these cell types, adequate nuclear AKG availability promotes DNA and histone demethylation, maintaining transcriptional programs associated with pluripotency, differentiation, and cellular homeostasis.
Mutations in the coding domain for IDH1 and IDH2 were reported to cause the production of the oncometabolite 2-hydroxyglutarate (2-HG) instead of AKG, resulting in abnormal cell proliferation in cancers like glioma and acute myeloid leukemia (AML). These mutations also resulted in epigenetic deregulation, as 2-HG can prevent histone demethylation by inhibiting AKG-dependent demethylases.
The TCA cycle intermediate α-ketoglutarate extends the lifespan of adult C. elegans. ATP synthase subunit beta is identified as a novel binding protein of α-KG. α-KG inhibits ATP synthase and, similar to ATP synthase knockdown, inhibition by α-KG leads to reduced ATP content, decreased oxygen consumption, and increased autophagy in both C. elegans and mammalian cells. The lifespan increase by α-KG requires ATP synthase subunit beta and is dependent on the target of rapamycin (TOR) downstream.
AKG affects the functioning of prolyl hydroxylases, which, in turn, influences the function of the hypoxia-inducible factor, an important transcription factor in cancer development and progression. As a substrate of hydroxylases belonging to OGDDs, AKG exerts an impact on prolyl/aspartyl/lysyl hydroxylations, which in turn regulates the stability of HIF-1 and collagen synthesis.
Leveraging Caenorhabditis elegans as a model system, Chin et al. uncovered a critical role of α-ketoglutarate (α-KG), a product of tricarboxylic acid metabolism, in prolonging life span. Supplementation of α-KG to the growth medium specifically prolonged the life span of worms by 50% and delayed their age-related phenotype.
Alpha-ketoglutarate (delivered in the form of a calcium salt, CaAKG), a key metabolite in the TCA cycle that is reported to extend lifespan in both C. elegans and Drosophila, can significantly extend lifespan and healthspan in mice. Basic research in the nematode worm C. elegans started AKG's journey to human clinical trials, noting that the first evidence that AKG extended lifespan in the microscopic worm came in 2014. Scientists tested AKG in distinct strains of the worm in 2017 and determined that treatment hit conserved aging pathways in the animals.
The pleiotropic functions of AKG suggest it may also extend human healthspan. Recent studies in worms and mice support this concept. However, a few studies published in the 1980s and 1990s in humans suggested the potential benefits of AKG in muscle growth, wound healing, and in promoting faster recovery after surgery. So far there are no recently published studies demonstrating the role of AKG in treating aging and age-related diseases; hence, further clinical studies are required to better understand the role of AKG in humans.
In a study of 42 individuals, Calcium alpha-ketoglutarate was shown to reduce biological age by up to 8 years with supplementation of 1 g for almost 7 months. This study (the "Rejuvant" study) assessed biological age using epigenetic clock measures. This is the form used in the ongoing ABLE placebo-controlled trial (1 g/day sustained-release).
The ABLE study is a double-blind randomized placebo-controlled study investigating the potential of Ca-Alpha-Ketoglutarate supplementation to reduce DNA methylation age and the effect on clinical and biological outcomes. ABLE is a double-blinded placebo-controlled randomized trial (RCT) of 1 g sustained-release Ca-AKG versus placebo for 6 months of intervention and 3 months follow-up including 120 40–60-year-old healthy individuals with a higher DNA methylation age compared to their chronological age.
Evidence characterization: The current AKG research presents a promising but still incomplete picture. The preclinical evidence is strong enough to justify continued interest. The biological mechanisms are plausible, and the early human findings provide enough support for further study. At the same time, the clinical evidence is not yet strong enough to make firm claims about AKG's effect on human aging.
Studies have revealed that αKG extends the lifespan of worms and maintains the pluripotency of embryonic stem cells (ESCs). Administration of αKG increases the bone mass of aged mice, attenuates age-related bone loss, and accelerates bone regeneration of aged rodents.
In humans, a key randomized controlled trial was conducted in postmenopausal women. A randomized, double-blind, placebo-controlled study with 76 postmenopausal women with osteopenia investigated the effect of Ca-AKG (6 g AKG and 1.68 g Ca per day) over a period of 6 months. The results showed a significant decrease in serum levels of C-terminal cross-linked telopeptide of type I collagen (CTX), a marker for bone resorption, by up to 37% after 24 weeks.
A study of post-menopausal women demonstrated that 6 g of Ca-AKG daily for 24 weeks reduced bone breakdown markers by 18% and improved lumbar bone mineral density by 1.6%. α-KG may be a therapeutic target for a variety of bone-related diseases, such as osteoporosis, osteoarthritis, and rheumatoid arthritis, because of its role in maintaining the metabolic balance of bone. As a potential therapeutic target for osteoporosis, osteoarthritis, and other diseases, α-KG needs more clinical trials to develop effective targeted drugs.
Evidence characterization: The bone health data in humans is drawn from a small number of controlled trials with limited sample sizes. Results are suggestive rather than conclusive; larger, longer trials are needed to confirm these effects.
As a precursor of glutamine, AKG supports the immune system and helps regulate protein metabolism, making it beneficial in states of increased protein catabolism, such as recovery from trauma or surgery. Clinical studies indicate its effectiveness in improving protein metabolism and reducing muscle proteolysis.
αKG dramatically increases the synthesis of arginine, proline, and polyamines and reduces oxidative stress, which also play a key role in metabolic adaptation before and after surgery.
One controlled trial that returned a null result is particularly informative: The aim of the study was to evaluate the feasibility of alpha-ketoglutarate enrichment of enteral feeding and the effect on protein metabolism after major surgery. Patients undergoing elective abdominal surgery were randomly allocated to receive a standard whole-protein-based enteral nutrition solution (n = 9) or an isonitrogenous, isocaloric solution enriched with alpha-ketoglutarate (n = 11) for 5 days postoperatively. There were no significant differences in nitrogen balance, excretion of 3-methylhistidine, or clinical outcome between groups. Enrichment of a whole-protein-based formula with alpha-ketoglutarate did not improve protein metabolism or decrease muscle catabolism after major abdominal surgery.
Despite indications in earlier literature, evidence supporting AKG's effect on muscle mass in healthy humans remains scarce.
Evidence characterization: Evidence for AKG in surgical recovery and protein metabolism is mixed. Some older trials and animal studies support a role; a more rigorously controlled clinical trial found no benefit for enteral enrichment after major abdominal surgery. Results may vary by form (OKG vs. free AKG), dose, and route of administration.
OKG is proposed to have potential therapeutic effects, particularly in stimulating muscle growth and preventing muscle breakdown, making it a focus of research for individuals recovering from trauma. The supplement is also considered for various health applications, including liver cirrhosis, prevention of muscle loss, immune system support, and gastrointestinal health.
People use ornithine ketoglutarate for healing wounds and burns. It is also used for building muscle strength, HIV/AIDS, stroke, and many other purposes, but there is no good scientific evidence to support these uses beyond burns. While there are anecdotal claims of its benefits in sports supplementation for muscle building, scientific evidence remains limited and primarily centered on its use in clinical recovery settings.
Evidence characterization: The most robust clinical data for OKG involves burn patients and post-trauma recovery settings, with moderate clinical evidence. Evidence for athletic or cosmetic uses is limited and primarily anecdotal.
Clinical studies with hemodialysis patients have shown that Ca-AKG at doses of up to 4.5 g/day for a period of up to three years is safe and can lead to an increase in plasma arginine levels and a decrease in plasma urea levels. Another older study in patients on hemodialysis found that calcium-alpha-ketoglutarate helped correct secondary hyperparathyroidism.
Evidence characterization: This is a specific clinical population (dialysis patients) and effects are not necessarily generalizable to healthy individuals. These studies also provide the longest-duration human safety data currently available.
Osteoarthritis (OA) is a degenerative disorder closely associated with aging and metabolic dysfunction, characterized by multiple pathological features, including cartilage degradation, inflammatory responses, cellular senescence, mitochondrial dysfunction, and ferroptosis. Recently, AKG has emerged as a promising therapeutic approach for OA. AKG restricts pro-inflammatory cytokine production, increases extracellular matrix synthesis, and reduces cartilage degradation in arthritic models.
Although recent studies suggest that DM-AKG possesses therapeutic potential in animal models of OA, including the attenuation of cartilage degeneration, suppression of lipid peroxidation, promotion of autophagy, and enhancement of cell survival, the majority of these findings are derived from in vitro experiments or animal studies. There is a clear absence of systematic clinical research on the use of AKG or its derivatives for the treatment of OA. Therefore, to evaluate its safety and efficacy in humans, further high-quality clinical trials are needed.
Evidence characterization: Preclinical and mechanistic data are promising; human clinical evidence is currently absent.
As a pivotal intermediate linking carbon and nitrogen metabolism, AKG plays a critical role in regulating fatty acid synthesis, glucose homeostasis, and amino acid metabolism. It has been reported to protect against a wide range of diseases such as cardiovascular, brain, and renal ailments. A study found that the plasma level of AKG was decreased in P407-induced hyperlipidemic mice and a 50 mg/kg daily dose of AKG reduced plasma lipid level, suggesting a link between AKG and lipid metabolism.
Evidence characterization: Primarily animal/in vitro data at this stage. Human clinical trials for cardiovascular outcomes have not been completed or published.
α-KG acts as a cofactor for a range of dioxygenases, including TET enzymes and JmjC domain-containing histone demethylases, which mediate DNA and histone demethylation, thereby regulating gene expression and cellular differentiation. Consequently, α-KG has emerged as a potential tumor suppressor by modulating dysregulated metabolic and epigenetic pathways in cancer cells.
Mutations in IDH genes lead to production of changed enzymes, which reduce AKG to another oncometabolite — R(−)-2-hydroxyglutarate (2HG). All the oncometabolites mentioned above modulate (inhibit) the activity of PHD, TET, and KDM enzymes and in this way they participate in the pathogenesis of many cancers.
Evidence characterization: The relationship between AKG and cancer is complex and context-dependent. AKG depletion (via IDH mutations) promotes cancer, while supplemental AKG may help restore epigenetic regulation in certain tumor types. This is an active area of basic and translational research; no clinical trials of AKG as an anticancer treatment in humans have been completed to date.
In research, the dosages used range from 3.6 g to 6 g, with higher dosing in people who have suffered burns, but a recommended daily dose has not yet been established. Since the effects are dose-dependent, finding an accurate dosing recommendation will be an important part of ongoing research.
The review highlights that AKG's safety record is strong, with doses up to 6 grams per day generally well tolerated. Clinical studies with hemodialysis patients have shown that Ca-AKG at doses of up to 4.5 g/day for a period of up to three years is safe.
High doses (over 5 to 10 g) can cause diarrhea and stomach cramps. The maximum safe dosages for young children, women who are pregnant or nursing, and those with serious liver or kidney disease have not been established.
The FDA has not tested alpha-ketoglutarate products to confirm that they contain the ingredients stated on their labels. Some dietary supplements have been tested by third-party organizations to confirm that they contain the ingredients listed on their labels and do not contain any harmful chemicals.
Alpha-ketoglutarate may be combined with other substances, including amino acids and minerals, to form combination ingredients such as AAKG, OKG, and Ca-AKG. These combination ingredients are intended to increase the levels of both substances in the body, and each of these substances can cause different effects and side effects.
Typical dosages for OKG range from 5 to 25 grams daily, though higher amounts may lead to digestive issues. While OKG appears to be safe for most, caution is advised for specific populations, including children and individuals with serious health conditions.
Ornithine ketoglutarate increases insulin, a hormone that regulates the amount of sugar in the blood, which is a pharmacodynamic consideration relevant to individuals managing blood glucose or taking diabetes medications.
One co-author of a key human supplementation review is a board member and equity holder at Ponce de Leon Health, a company aimed at developing nutritional supplements for aging, which manufactures several products related to AKG. Readers should be aware of this when evaluating the strength of claims made in that review.
Even though many compounds have been tested in animal models, the translation to humans is limited. Alpha-Ketoglutarate has been studied widely in model animals, but there are few studies testing its geroprotective properties in humans. The body of rigorous human RCT data remains limited as of 2024–2025, and results from several ongoing trials (including ABLE) are needed before clinical recommendations can be firmly established.
Health conditions that AKG (alpha-ketoglutarate) may help support.
AKG is recognized as an endogenous antioxidant: it scavenges reactive oxygen species (ROS), restores antioxidant enzyme activities (SOD, glutathione peroxidase), and reduces lipid peroxidation products in the liver and kidneys. The 2022 Trends Endocrinol Metab review (Gyanwali et al.) explicitly classifies AKG as an antioxidant that affects epigenetic and immune regulation.
A 2025 PMC review specifically analyzed AKG's mechanisms in osteoarthritis (OA), documenting its roles in autophagy regulation, gut microbiota modulation, cellular senescence reduction, and ferroptosis inhibition in chondrocytes. A 2026 MDPI review notes AKG restricts pro-inflammatory cytokine production and reduces cartilage degradation in arthritic models. Human clinical data in arthritis specifically are not yet published.
Alpha-ketoglutarate (AKG) is a Krebs cycle intermediate and nitrogen acceptor involved in glutamate and glutamine synthesis. Used in clinical and sports nutrition contexts as ornithine alpha-ketoglutarate (OAK) or arginine alpha-ketoglutarate (AAKG) for muscle protein synthesis support and recovery. The EBSCO Research Starters sports performance database lists it as a proposed ergogenic aid.
Ca-AKG has been tested in a human RCT in postmenopausal women (6 g/day for 6 months), showing reduced bone resorption markers and modest improvements in lumbar bone mineral density. AKG acts as a cofactor for prolyl hydroxylase, which is essential for collagen stabilization in bone matrix. Animal models confirm AKG increases bone mass and attenuates age-related bone loss via histone methylation regulation of BMP signaling.
Alpha-Ketoglutarate (AKG) is a key TCA cycle intermediate that directly sustains mitochondrial energy flux, facilitates amino acid metabolism feeding into the cycle, and serves as a substrate for cellular ATP production. Supplemental AKG has been shown to support energetic capacity and has clinical use in critical care and aging.
AKG suppresses the NF-κB-mediated inflammatory pathway and reduces pro-inflammatory cytokine production across multiple model systems. In mice, Ca-AKG supplementation lowered systemic inflammatory markers including pro-inflammatory cytokines while raising anti-inflammatory IL-10. Human mechanistic evidence is indirect, derived from clinical nutrition contexts where AKG modulates immune and inflammatory signaling.
AKG is a TCA cycle intermediate that declines ~10-fold between ages 40 and 80 in humans. A human study in 42 adults (mean age 64) supplementing with Ca-AKG for ~7 months reported an average 8-year reduction in DNA methylation biological age. Preclinical evidence shows Ca-AKG rescues synaptic plasticity deficits in Alzheimer's mouse models and improves cognitive function via mTOR pathway modulation.
AKG is a required cofactor for prolyl hydroxylases, the enzymes that hydroxylate proline residues to stabilize triple-helical collagen. Without adequate AKG, collagen in bones, skin, tendons, and other connective tissues becomes less stable. This biochemical role is well established and underpins AKG's effects across multiple connective-tissue-rich systems.
Alpha-ketoglutarate (AKG) is an intermediate in the TCA (Krebs) cycle and plays a central role in cellular energy production. It also serves as a nitrogen scavenger and is involved in amino acid synthesis. Emerging clinical evidence in older adults suggests AKG supplementation may support energy metabolism and reduce age-related metabolic decline.
Alpha-ketoglutarate (AKG), a key Krebs cycle intermediate, is a component of OKG and has been studied for its role in amino acid metabolism and anabolic hormone (including GH) secretion. As part of OKG, AKG contributes to the compound's established GH-stimulating properties. AKG's independent role in GH secretion is based partly on its metabolic precursor relationship to arginine and glutamine, which are documented GH secretagogues.
Alpha-ketoglutarate is a key intermediate in the Krebs cycle and a cofactor for epigenetic enzymes (TET demethylases, histone demethylases) that regulate aging-associated DNA methylation patterns. A 2020 RCT in humans found calcium alpha-ketoglutarate supplementation reduced biological age by 8 years as measured by DNA methylation clocks in middle-aged adults.
Alpha-ketoglutarate (AKG) is a key TCA cycle intermediate and precursor to several amino acids. Supplemental AKG has been studied for improving mitochondrial energy metabolism, supporting anabolism in critical illness, and is used in the context of aging interventions targeting mitochondrial metabolic efficiency.
AKG supports muscle recovery through multiple mechanisms: it is a nitrogen scavenger, a precursor of glutamine and glutamate, stimulates protein synthesis, inhibits protein degradation, and activates muscle satellite cells. A 2024 MDPI narrative review of 112 peer-reviewed studies confirmed that AKG reduces fatigue and supports faster post-exercise recovery. A double-blind RCT in untrained young men found improved training tolerance with alpha-keto acid supplementation.
AKG and its calcium salt (Ca-AKG) have demonstrated anti-osteoporotic effects in both human trials and animal models. In postmenopausal women, Ca-AKG 6 g/day for 6 months reduced bone resorption marker CTX and improved lumbar BMD. In aged mice, AKG attenuated age-related bone loss by reducing senescence of bone marrow mesenchymal stem cells via histone demethylation.
Alpha-ketoglutarate (AKG) is a key TCA cycle intermediate and glutamine precursor that supports cellular energy production and nitrogen metabolism during physical exercise. It has been studied as an ergogenic aid, particularly in combination with amino acids, showing improvements in exercise performance and muscle recovery. It reduces ammonia accumulation, which contributes to fatigue during prolonged exercise.
Clinical studies since the 1980s and 1990s have used AKG—primarily in its ornithine salt form (OKG)—to improve nitrogen balance, protein status, and recovery outcomes in surgical, traumatic, and burn patients. AKG facilitates muscle protein synthesis and nitrogen conservation in post-operative states. The AEGIS trial is currently evaluating 1 g Ca-AKG for enhanced surgical recovery.
AKG is a required cofactor for prolyl hydroxylases that stabilize collagen. In cultured human dermal fibroblasts, AKG stimulated procollagen production by ~25.6%. Topical hexyl ester of AKG reduced UV-induced wrinkle formation in mice and improved elasticity in a small human volunteer study. AKG levels in plasma correlate with skin health in aging models.
OKG (ornithine alpha-ketoglutarate) has demonstrated accelerated wound healing in multiple RCTs in burn patients, and in four controlled trials in elderly patients with pressure ulcers. The mechanism involves enhanced nitrogen balance, increased synthesis of proline (for collagen), glutamine (immune fuel), and arginine, plus anabolic hormone stimulation. AKG is also used in clinical wound-healing formulations.
Body systems that AKG (alpha-ketoglutarate) may help support.
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