IngredientsSuccinic acid is a dicarboxylic acid with the chemical formula (CH₂)₂(CO₂H)₂. Known as butanedioic acid or amber acid, and as succinate in its anionic form, it is classified as a dicarboxylic acid. Its CAS number is 110-15-6. It is known by numerous synonyms in the scientific and regulatory literature, including butanedioic acid, amber acid, wormwood acid, Asuccin, dihydrofumaric acid, Katasuccin, Succinicum acidum, Acidum succinicum, acide succinique (French), and Bernsteinsäure (German).
Succinic acid is composed of four carbon atoms, six hydrogen atoms, and four oxygen atoms (C₄H₆O₄) and appears as colorless crystals, highly soluble in water. The name "succinic" derives directly from its most celebrated natural source: it is found in small amounts in plants, animals, and fermented products, and is especially concentrated in amber, from which its name is derived — succinum is Latin for amber.
Succinic acid is distributed widely through the natural world — especially in amber (3–8% by weight) and in plant and animal tissues, and in microorganisms. It plays a significant role in intermediary metabolism, mainly in the TCA (Krebs) cycle and the glyoxylate pathway.
Baltic amber contains 3–8% of succinic acid by weight. The highest content of the acid is found in the amber cortex — the external layer of the stone. Baltic amber is the richest known natural exogenous source; it is a specific subset of amber found only in northern Europe, mainly in the areas surrounding the Baltic Sea, with resin found in Poland, Lithuania, Latvia, Estonia, Sweden, and as far west as the United Kingdom. Baltic amber accounts for over 90% of the world's known amber today.
Traditionally, succinic acid was extracted by distilling amber. Today, production methods have modernized and diversified. Industrial production now relies primarily on microbial fermentation, including metabolically engineered strains such as Actinobacillus succinogenes, which can utilize renewable feedstocks such as lignocellulosic hydrolysate derived from agricultural residues. Succinic acid is an industrially important component that plays a key role in food additives, dietary supplements, and precursors for biodegradable polymers.
As a dietary supplement, succinic acid is available in multiple forms:
As a food additive and dietary supplement, succinic acid is generally recognized as safe (GRAS) by the U.S. Food and Drug Administration. It is used primarily as an acidity regulator in the food and beverage industry and is also available as a flavoring agent, contributing a somewhat sour and astringent component to umami taste. Succinic acid is marketed as food additive E363.
As an excipient in pharmaceutical products, it is also used to control acidity or as a counter-ion. Drugs that include formulations of their active ingredients as succinate salts include metoprolol succinate, sumatriptan succinate, doxylamine succinate, and solifenacin succinate.
The use of amber, which contains succinic acid, dates back thousands of years in European and Asian traditional medicine. Baltic amber was worn as jewelry or applied to the skin in the belief that it promoted healing, pain relief, and protection.
Hippocrates (460–377 BC), the father of medicine, described in his works the medicinal properties and methods of application of Baltic amber, which were later used by scientists until the Middle Ages. In ancient Rome, amber was used as medicine and as protection against various diseases. The physician Calistratus wrote that amber protects from madness, that powder of amber mixed with honey cures throat, ear, and eye diseases, and that taken with water it cures stomach illnesses.
Pliny the Younger noted that Roman peasant women wore amber medallions not only as adornments, but also as a remedy for swollen glands and sore throat and palate. The Persian scientist Ibn Sina (Avicenna) called natural amber a remedy for many diseases. There was a belief in Eastern countries that amber smoke strengthens the human spirit and gives courage. In Asian countries, an "amber syrup" — a mixture of succinic acid (amber acid) and opium — was used as a tranquilizer and antispasmodic.
In ancient Rome, amber was used as a medicine and protection against various diseases. The physician of that time, Calistratus, wrote that amber protects against madness, and amber powder mixed with honey cures diseases of the throat.
Amber was historically applied in various preparations including powder, chips, and infused oils applied to the body. In Eastern Europe and Russia, succinic acid (particularly from amber extracts) has been used in folk and medical traditions to support stress reduction, inflammation control, and general vitality.
As a chemical compound in its isolated form, succinic acid is one of the oldest biologically active additives, identified as early as the 17th century. The substance, obtained by the German doctor I. K. Barkhausen (1666–1723) as a result of the distillation of Baltic sunstones, appeared as tiny colorless crystals that dissolved well in water and alcohol.
Notably, Nicolaus Copernicus documented that his formulas for medicine included 22 specific ingredients — and one of them was amber.
Amber powder or oil infusions were applied to treat rheumatic pain, respiratory infections, and skin inflammation. Amber teething necklaces have also been used historically to soothe infants.
Succinic acid was analyzed in 1886 by the pioneer of modern bacteriology and Nobel Prize-winner Robert Koch, who confirmed its positive influence, discovering that there is no risk of the accumulation of surplus amounts of succinic acid in the human organism, even after the introduction of considerable amounts into the body.
In the 1920s, succinate was first correlated to a carbohydrate oxidation sequence proposed by Thorsten Thunberg. In the following decade, this sequence of oxidation was better described thanks to Albert von Szent-Györgyi's studies on pigeon breast muscle. These observations laid the foundation for Hans Krebs's later formulation of the tricarboxylic acid cycle.
For many decades, succinate (succinic acid at blood pH) was considered only as an intermediate metabolite of the TCA cycle. During aerobic respiration, succinate is oxidized to fumarate, donating reducing equivalents. The reaction is catalyzed by succinate dehydrogenase (SDH), an enzyme complex located in the inner mitochondrial membrane that participates in both the TCA cycle and the electron transport chain.
At its core, succinic acid (or its anionic form, succinate) is a critical intermediate in the citric acid cycle, the central hub of cellular respiration where nutrients are broken down to generate ATP, the cell's primary energy currency. Succinate dehydrogenase converts succinate to fumarate, linking the cycle to the electron transport chain. This metabolic role means that succinic acid is intrinsically tied to energy production and cellular function. Disruptions in succinate metabolism can therefore lead to significant cellular dysfunction, observed in certain mitochondrial diseases.
Beyond its role in energy metabolism, succinate has emerged as a crucial signaling molecule. It can be released from mitochondria into the cytoplasm and even the extracellular space, where it acts as a messenger.
Succinate acts as an extracellular ligand by binding to a G-protein coupled receptor known as GPR91 (also called SUCNR1), expressed in kidney, liver, heart, retinal cells, and possibly many other tissues, leading to a wide array of physiological and pathological effects. Through GPR91, succinate is involved in functions such as regulation of blood pressure, inhibition of lipolysis in white adipose tissue, development of retinal vascularization, cardiac hypertrophy, and activation of stellate hepatic cells by ischemic hepatocytes.
Succinate inhibits the action of prolyl hydroxylases (PHD) and thereby causes stabilization of hypoxia-inducible factor-1α (HIF-1α). This is a pivotal finding from landmark research published in Nature (Tannahill et al., 2013), which demonstrated that intracellular succinate promotes the stabilization of HIF-1α and enhances proinflammatory IL-1β production, and that increased intracellular succinate promotes IL-1β transcription via stabilization of HIF-1α after LPS stimulation.
When SUCNR1/GPR91-expressing macrophages are activated by inflammatory signals, they change their metabolism and accumulate succinate. During this activation, macrophages release succinate into the extracellular milieu. They simultaneously up-regulate GPR91, which functions as an autocrine and paracrine sensor for extracellular succinate to enhance IL-1β production.
This dual role — succinate both driving and potentially modulating inflammation depending on context — is an area of active research. The TCA cycle intermediate succinate is released from cells under metabolic stress and has recently emerged as a metabolic signal induced by proinflammatory stimuli.
Electrons from the oxidation of NADH are routed through Complex I to coenzyme Q, whereas electrons from the oxidation of carbon fuel substrates in the citric acid cycle that reduce FAD are funneled to ubiquinone through Complex II (succinate dehydrogenase). SDH catalytic activity is also modulated by Krebs cycle intermediates including oxaloacetate, which is a potent inhibitor. Succinate promotes the dissociation of oxaloacetate from SDH, thereby activating the enzyme.
Elevated succinate also drives ROS production through a mechanism called reverse electron transport (RET). When the mitochondrial respiratory chain is oxidizing high levels of succinate under conditions of high protonmotive force — for example, when mitochondria are not making much ATP — the CoQ pool becomes reduced, leading to reversal of the normal direction of electron flow through complex I. As RET leads to dramatic production of ROS, RET enables mitochondria to release a variable redox signal that can respond sensitively to mitochondrial status.
This mechanism is particularly relevant in ischemia-reperfusion injury: during ischemia, succinate accumulation followed by rapid re-oxidation upon reperfusion has been linked to increased production of reactive oxygen species (ROS), contributing to tissue injury.
The link between succinic acid levels and various health conditions is a growing area of research. Dysregulation of succinate metabolism has been implicated in several pathologies, including certain types of cancer (where it is considered an oncometabolite) and conditions associated with hypoxia or mitochondrial dysfunction. Increased succinate levels can inhibit enzymes involved in epigenetic regulation, leading to altered gene expression patterns that can promote tumorigenesis.
High succinate concentrations have been detected in the plasma of patients with peritonitis, and in the urine and plasma of diabetic and metabolic disease rodent models. Patients harboring mutations in SDH have increased HIF-1α activity and circulating succinate.
It is known that succinic acid can penetrate the blood-brain barrier, and exogenous treatment with succinic acid exerts ameliorative effects on mitochondrial dysfunction and neurodegenerative ataxia. Moreover, succinic acid derivatives — such as emoxipine, reamberin, and mexidol — exert acute antidepressant effects by inhibiting monoamine oxidase activity.
This is the area with the strongest human clinical trial data for succinic acid as a dietary supplement ingredient. Multiple randomized, double-blind, placebo-controlled trials (RCTs) have been conducted using an ammonium succinate-based multi-ingredient supplement.
A pooled analysis of two identical randomized, double-blind, placebo-controlled clinical trials of a succinate-based dietary supplement for menopausal symptoms was published in Obstetrics and Gynecology International (2019) by Radzinsky et al. Across these trials, women taking the succinate-based formulas experienced reduced frequency and severity of hot flashes and night sweats, as well as improvements in mood, anxiety scores, and sleep quality.
These formulations usually combined ammonium succinate or other succinate salts with minerals (such as calcium, magnesium, zinc), amino acids (like glycine), and vitamin E, and were typically taken once or twice daily for several months. They were studied in women with mild to moderate vasomotor and psychosomatic menopausal symptoms.
The proposed mechanism is linked to the hypothesis that deficit in estrogen stimulation leads to a decrease in energy production in neurons, which in turn causes neuronal dysregulation. Vasomotor instability, psychosomatic symptoms, and sleep disturbances can result from above-mentioned neuronal dysregulation; the use of ammonium succinate, which targets mitochondria, may be able to restore some of the energy deficit resulting from low estrogen levels in the CNS.
Evidence strength: Moderate. The trials used validated outcome measures (Greene Climacteric Scale, STAI questionnaire), had identical protocols, and were placebo-controlled. However, succinic acid was always tested as part of a multi-ingredient formulation, making it impossible to isolate the contribution of succinic acid alone. The trials were primarily conducted in Russian-speaking populations and were sponsored by the manufacturer of the supplement, a limitation acknowledged in the disclosures.
Antioxidants may have a positive impact on diabetic polyneuropathy (DPN), presumably due to alleviation of oxidative stress. The CYLINDER trial aimed to evaluate the efficacy and safety of a combination of antioxidants — succinic acid, inosine, nicotinamide, and riboflavin (SINR) — in the treatment of DPN. In this double-blind, placebo-controlled clinical trial, men and women aged 45–74 years with type 2 diabetes and symptomatic DPN (with initial Total Symptom Score >5) were randomized into experimental (n=109) and control groups.
A 3-month treatment with a combination of riboflavin, inosine, succinic acid, and nicotinamide was found to help reduce numbness, burning, and paresthesia in patients with diabetic polyneuropathy (Kharitonova et al., 2022). The trial was published in BMJ Open Diabetes Research & Care (2022).
Evidence strength: Preliminary. The study was multicenter and placebo-controlled, but succinic acid was administered as part of a four-component combination; the isolated contribution of succinic acid to symptom improvement cannot be determined from this trial. The study was funded by POLYSAN Scientific & Technological Pharmaceutical Company, and several investigators had financial relationships with the sponsor.
This is an emerging and growing area of application. As of February 2026, there is no comprehensive review specifically addressing the application of succinic acid and its derivatives in cosmetology, cosmetic formulations, and aesthetic dermatology. A 2026 review in Applied Sciences (MDPI) provides analysis of succinic acid, from its chemical structure and role in energy metabolism to its multidimensional clinical applications, with particular emphasis on the synergy between sodium succinate and hyaluronic acid in treating acne and minimizing post-procedural inflammations.
Acne: Succinic acid, a short-chain fatty acid, is produced during fermentation by commensal bacteria such as Staphylococcus epidermidis found on the skin. This acid has been shown to inhibit C. acnes growth, thereby reducing acne-related inflammation. Topical and intralesional applications of succinic acid have demonstrated effectiveness in suppressing C. acnes-induced inflammation both in vitro and in vivo. These findings suggest that succinic acid not only modulates the skin's microbiome but also holds promise as a therapeutic agent in acne treatment.
Exfoliation and barrier function: A 2026 study in Cosmetics (MDPI) systematically evaluated bio-based succinic acid (bSU) against salicylic acid using reconstructed human epidermis and human skin explants. Results positioned bio-based succinic acid as a balanced exfoliating bioactive that effectively promotes stratum corneum renewal while preserving cutaneous barrier homeostasis.
Chemical peels: As a chemical peel, succinic acid represents an innovative alternative to classic hydroxy acids. Its superficial action is based on gentle exfoliation coupled with intensive anti-inflammatory and antioxidant effects, making it an ideal tool for treating acne-prone, vascular, and reactive skin. Unlike aggressive exfoliating acids, succinic acid promotes the structural renewal of the epidermis without inducing excessive trauma.
Anti-inflammatory limitations in topical use: Evidence here is mixed and must be noted honestly. A study on amber teething necklaces revealed that there was no solid evidence that succinic acid has anti-inflammatory effects when applied topically to the skin. Moreover, tests on macrophages showed that succinic acid did not result in a reduction of inflammatory cytokines and could even be toxic at high concentrations.
Rosacea and erythema: Rosacea remains one of the most challenging conditions in cosmetic dermatology due to its sensitivity and vascular component. Published clinical work in the Journal of Cosmetic Dermatology highlights succinic acid's potential to reduce erythema, improve skin tolerance, and enhance overall skin quality. These effects are likely linked to its ability to modulate inflammatory signaling, support mitochondrial resilience, and improve vascular balance.
Skin hydration and hyperpigmentation: The antioxidant activity of succinic acid protects cells against oxidative stress — one of the key mechanisms involved in the development of skin discoloration. An additional advantage of succinic acid is its ability to modulate the immune response and reduce inflammatory processes through the downregulation of pro-inflammatory cytokines. It also enhances microcirculation and supports neoangiogenesis, contributing to improved tissue oxygenation and regenerative capacity.
Evidence strength: Preliminary to moderate. Most dermatology evidence is derived from in vitro studies, reconstructed skin models, or small uncontrolled clinical observations. Large, well-powered randomized controlled trials in dermatological populations are lacking.
In preclinical research, succinum (amber) extracts were investigated for anti-neuroinflammatory effects in BV2 microglial cells exposed to LPS and for antidepressant-like activity in mice. As an alternative and complementary medicine, Pinus spp. succinum has been prescribed for alleviating brain disorders and emotional abnormalities.
It is known that succinic acid can penetrate the blood-brain barrier, and exogenous treatment with succinic acid exerts ameliorative effects on mitochondrial dysfunction and neurodegenerative ataxia. Moreover, succinic acid derivatives such as emoxipine, reamberin, and mexidol exert acute antidepressant effects by inhibiting monoamine oxidase activity.
Evidence strength: Weak for succinic acid itself; most evidence is animal or in vitro. Its derivatives used in Russian clinical pharmacology (reamberin, mexidol) have been studied in humans, but these are structural analogues, not succinic acid per se. No large-scale RCTs in human neurological disorders have been conducted using isolated succinic acid supplements.
The TCA cycle intermediate succinate is released from cells under metabolic stress and has recently emerged as a metabolic signal induced by proinflammatory stimuli. Research has investigated whether succinate receptor 1 (SUCNR1) plays a role in the development of adipose tissue inflammation and type 2 diabetes.
Circulating succinate is elevated in rodent models of hypertension and metabolic disease. Through GPR91/SUCNR1, succinate is involved in functions such as regulation of blood pressure, inhibition of lipolysis in white adipose tissue, and development of retinal vascularization.
Evidence strength: Mechanistic and preclinical. These findings are derived from rodent models and cell-based assays. There are no completed clinical trials examining oral succinic acid supplementation in cardiovascular disease or type 2 diabetes management in humans.
Extracellular succinate levels within the synovial fluid of arthritic joints activate macrophages via GPR91 to up-regulate IL-1β production. Research revealed a GPR91/succinate-dependent feed-forward loop of macrophage activation, with the authors proposing GPR91 antagonists as novel therapeutic principles to treat rheumatoid arthritis.
Evidence strength: Preclinical. The mechanistic data are compelling and published in high-quality journals (Journal of Experimental Medicine), but translational studies targeting the GPR91 axis with exogenous succinic acid in human RA patients are not yet available.
A frequently cited use is wearing Baltic amber teething necklaces for infant teething pain. The proposed mechanism is that body heat releases succinic acid from the amber beads, which is then absorbed transdermally. A study in 2019 found that succinic acid could not be released from Baltic amber beads into human skin, and also found no approved anti-inflammatory properties for this mode of delivery. The same study revealed no solid evidence that succinic acid has anti-inflammatory effects when applied topically to the skin; tests on macrophages showed that succinic acid did not result in a reduction of inflammatory cytokines and could even be toxic at high concentrations.
Evidence strength: Negative/absent. Available evidence does not support the biological plausibility of this application.
No universal standardized dosage has been established for succinic acid as a standalone dietary supplement. Dosages vary significantly by application and formulation.
Overall, succinic acid's benefits are promising but should be considered "supportive" rather than curative. Robust evidence exists mainly for specific succinate-based products under trial conditions, not for unrestricted use of standalone succinic acid in every context. People take succinate for symptoms of menopause, obesity, and sexual problems, but there is no good scientific evidence to support these uses.
As a food additive and dietary supplement, succinic acid is generally recognized as safe by the U.S. Food and Drug Administration. Its safety as a food additive has been approved by the U.S. Food and Drug Administration (FDA), European Food Safety Authority (EFSA), and the Joint FAO/WHO Expert Committee on Food Additives (JECFA), as well as other authorities.
When taken by mouth, the succinic acid form of succinate is likely safe when used in the amounts found in foods. There is not enough reliable information to know if succinate or succinic acid are safe or what the side effects might be when they are used in medicinal amounts.
From a biochemical perspective, succinate is an endogenous compound produced naturally in human metabolism, which some argue supports its general safety profile. However, the relevance of natural occurrence to food additive safety is subject to scientific debate and does not inherently guarantee safety at elevated dietary levels.
Succinic acid has been found to inhibit the activity of cytochrome P450 (CYP450) enzymes (Wang H, Xia B, Lin M, et al.). CYP450 enzymes are central to the hepatic metabolism of a large number of pharmaceutical drugs. This finding carries potential implications for drug interactions in individuals taking medications metabolized by CYP450 pathways, though clinical significance in humans at supplemental doses has not been quantified in the available literature.
Tests on macrophages showed that succinic acid could be toxic at high concentrations. This is relevant primarily for topical concentrations in cosmetic formulations and informs the dose ranges used in peel procedures.
The immunological profile of succinic acid/succinate is context-dependent and not straightforwardly anti-inflammatory. LPS-activated inflammatory (M1) macrophages display a broken Krebs cycle, which ultimately causes intracellular succinate accumulation. Furthermore, intracellular succinate promotes the stabilization of HIF-1α and enhances proinflammatory IL-1β production. This means that under certain inflammatory conditions, elevated succinate can aggravate rather than resolve inflammation — a nuance that is often overlooked in supplement marketing.
Reverse electron transport driven by the oxidation of succinate has been proposed as the mechanism of accelerated production of reactive oxygen species in post-ischemic mitochondria. In neonatal mouse models of hypoxic-ischemic brain injury, at initiation of reperfusion, brain mitochondria demonstrated Complex II-dependent respiration, associated with a 30-fold increase in cerebral succinate concentration and significantly elevated H₂O₂ emission rate compared to controls. While this is relevant to pathophysiology rather than supplement safety per se, it underscores that unnaturally elevated succinate can drive oxidative damage in specific clinical contexts.
Disodium succinate has not received GRAS status from the U.S. FDA. This means it does not qualify for the simplified regulatory pathway available to GRAS substances and requires full food additive approval procedures if used in the United States. The lack of GRAS designation does not automatically indicate the substance is unsafe; rather, it reflects that the FDA has not made a GRAS determination based on available evidence. Regulatory status varies internationally, and some countries and regions may permit disodium succinate under different classification systems or with specific usage limitations.
Succinate activates HIF-1α in tumours, indicating an important similarity between inflammation and cancer. The inflammatory process may have a tumorigenic effect by increasing succinate. The identification of succinate as a danger signal may therefore be important for understanding innate immunity in both inflammatory diseases and cancer. This remains a preclinical concern rather than a demonstrated clinical risk from dietary supplementation, but it is scientifically relevant and warrants monitoring in future research.
Health conditions that Succinic acid may help support.
Succinic acid, produced by commensal skin bacteria such as Staphylococcus epidermidis, inhibits Cutibacterium acnes growth and reduces acne-associated inflammation in vitro and in vivo. Topical and intralesional applications have demonstrated antimicrobial and anti-inflammatory activity against acne-triggering bacteria. Its tolerability advantage over salicylic acid makes it an emerging option for sensitive acne-prone skin.
Succinic acid reduces lipid peroxidation, modulates reactive oxygen species production, and in animal models demonstrates antihypoxic and antioxidant effects. In oxidant-injured cells, succinate supplementation reduced lipid peroxidation 2-fold compared to controls. The 2026 exercise systematic review also found improved antioxidant status in athletes.
Succinic acid directly enters the electron transport chain at Complex II, generating FADH2 and driving ATP synthesis independently of Complex I. This bypass property has been exploited in preclinical models of mitochondrial dysfunction to rescue cellular ATP levels. It is the most mechanistically established of all succinic acid–related health relationships.
In HFD-induced obese mice, succinic acid supplementation decreased serum TG, TC, and LDL-C while increasing HDL-C. Menopausal RCTs also assessed apolipoprotein A1 and B levels and reported favorable changes. Evidence is currently limited to animal and perimenopausal studies.
In menopausal RCTs, fatigue was among the symptom domains significantly improved by succinate-based supplementation. As a direct mitochondrial substrate entering oxidative phosphorylation via Complex II, succinic acid provides a mechanistic basis for combating cellular energy deficits. Animal studies confirm succinate rescues ATP levels under metabolic stress conditions.
Succinic acid acts as an extracellular signaling molecule through the G-protein–coupled receptor SUCNR1 (GPR91), modulating macrophage polarization and downstream inflammatory cytokine production. Succinate accumulation during inflammatory states stabilizes HIF-1α, amplifying IL-1β secretion in macrophages. This dual pro- and anti-inflammatory signaling role makes the relationship complex and context-dependent.
Succinic acid is a central intermediate of the mitochondrial TCA cycle, donating electrons directly to Complex II of the electron transport chain to drive ATP synthesis. Animal and in vitro studies confirm it sustains mitochondrial respiration and increases ATP production under metabolic stress. A 2026 systematic review of human exercise studies found mixed but suggestive evidence for improved oxygen uptake and aerobic performance.
Ammonium succinate–based dietary supplements have been tested in multiple randomized, double-blind, placebo-controlled trials in perimenopausal and postmenopausal women and significantly reduced hot flushes. A pooled analysis of two RCTs (n=227) found significant alleviation of 16 of 21 menopausal symptoms on the Greene Climacteric Scale. Estradiol levels also increased significantly.
In HFD-induced obese mice, succinic acid supplementation (40 mM) enhanced insulin sensitivity and improved glucose tolerance via PGC-1α/UCP1 adipose browning. A rat study using an oleic acid–succinic acid combination showed a 35.69% reduction in blood glucose levels. However, a separate mouse study found no effect on in vivo insulin tolerance, reflecting context-dependent results.
Succinate-based dietary supplements have been evaluated in several RCTs in perimenopausal and postmenopausal women, demonstrating improvements across vasomotor, psychological, and somatic symptom domains. Effects include reduced anxiety, improved body weight markers, and increased estradiol. A 2024 Advances in Therapy trial further evaluated Amberen combined with B vitamins in perimenopause.
Succinic acid–based supplements improved body weight, waist circumference, and apolipoprotein levels in menopausal RCTs, and animal studies show favorable effects on central adiposity, lipid profiles, and adipose tissue metabolism. The SUCNR1 signaling pathway links succinate to adipose inflammation and glucose intolerance relevant to metabolic syndrome.
In rodent models, succinic acid supplementation enhances fat metabolism by promoting white adipose tissue browning, reducing adiposity, and improving lipid profiles. One mouse study (PMC, 2024) found decreased serum TG, TC, and LDL-C alongside increased HDL-C. Mechanisms involve PGC-1α/UCP1 signaling via P38/MAPK and increased mitochondrial biogenesis.
Succinic acid is the canonical substrate of mitochondrial Complex II (succinate dehydrogenase), directly supporting oxidative phosphorylation. In cell and animal models, exogenous succinate rescues mitochondrial energy deficits under oxidant injury, hypoxia, and Complex I inhibition. Animal studies also suggest succinic acid promotes mitochondrial biogenesis in skeletal muscle.
A 2026 PRISMA systematic review of human exercise studies found that succinate-containing supplements improved acid-base regulation, oxygen transport hematological markers, and antioxidant status in athletes. Three of six included studies reported improvements in maximal oxygen uptake and anaerobic threshold power. Evidence quality is limited by high risk of bias and use of multi-ingredient formulations.
Succinic acid enhances mitochondrial activity in skin cells, supporting cellular energy production necessary for collagen synthesis and epidermal renewal. Supplier-commissioned studies suggest it inhibits collagen-degrading enzymes and reduces lipid peroxidation, providing antioxidant and anti-aging effects. Evidence is predominantly from in vitro and cosmetic ingredient studies rather than controlled clinical trials.
In RCTs of succinate-based dietary supplements for menopausal syndrome, significant reductions in anxiety and improvements in stress resilience and psychological adaptability were measured using the Spielberger-Hanin State-Trait Anxiety Inventory. Traditional use has also described succinic acid, historically derived from amber, as a nervous system tonic used to relieve stress.
Succinic acid has been shown to accelerate injured tissue regeneration and support wound repair by enhancing mitochondrial energy production in repair-active cells and modulating inflammatory resolution. In vitro and preclinical data show reduced cell lysis in oxidant-injured cells supplemented with succinate. Topical succinic acid is also noted for supporting wound healing in acne and skin lesion contexts.
Body systems that Succinic acid may help support.
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