판토텐산

Yellow viscous oil

Viscous oil

Viscous hygroscopic liquid

Soluble

Very soluble in water, benzene, ethyl ether

Freely soluble in water, ethyl acetate, dioxane, glacial acetic acid; Moderately soluble in ether, amyl alcohol. Practically insoluble in benzene, chloroform.

1000.0 mg/mL

195ºC (D-Calcium Pantothenate salt)

MELTING POINT: 170-172 °C /CA SALT/

< 25 °C

Very hygroscopic crystals. Specific optical rotation: + 27.1 deg at 25 °C/D (C = 2) /Pantothenic acid, sodium salt/

Minute needles from methyl alcohol; sweetish taste with slightly bitter aftertaste; decomposes 195-196 °C; moderately hygroscopic. Specific optical rotation: +28.2 deg at 25 °C/D (c = 5). 1 g dissolves in 2.8 mL water. Soluble in glycerol; slightly soluble in alcohol, acetone. pH of 5% aq soln: 7.2 - 8.0; pH in CO2-free water: 8.7 /Calcium salt/

Specific optical rotation: 37.5 deg at 25 °C/D

Viscous liquid; Unstable and extremely hygroscopic; [Merck Index]

Solid

Unstable ... easily destroyed by acids, bases, heat

Pantothenoic acid occurs as an unstable, hygroscopic, viscous oil which is freely soluble in water.

151.2 Ų [M+Na]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID4047173]；147.1 Ų [M-H]- [CCS Type: DT; Buffer gas: N2; Ionization: ESI-; Dataset: TOXCAST; Source Identifier: DTXSID4047173]

146.6 Ų [M-H]- [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]；150.8 Ų [M+Na]+ [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]；129.9 Ų [M+H]+ [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]

150.17 Ų [M+H]+ [CCS Type: DT; Method: stepped-field]；155.27 Ų [M+Na]+ [CCS Type: DT; Method: stepped-field]；149.87 Ų [M-H]- [CCS Type: DT; Method: stepped-field]

148.1 Ų [M+H]+ [CCS Type: DT; Method: single field calibrated with Agilent tune mix (Agilent)]

145 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine]

146.6 Ų [M-H]-；203 Ų [M+H]+；129.8 Ų [M+H]+；150.8 Ų [M+Na]+

1 G EQUALS 70,000-75,000 CHICK UNITS

Extremely hygroscopic

This chemical does not meet GHS hazard criteria for 100% (3 of 3) of all reports.

Not Classified；Reported as not meeting GHS hazard criteria by 3 of 3 companies. For more detailed information, please visit ECHA C&L website.

Aggregated GHS information provided per 3 reports by companies from 1 notifications to the ECHA C&L Inventory.；Reported as not meeting GHS hazard criteria per 3 of 3 reports by companies.；There are 0 notifications provided by 0 of 3 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Chemical: .beta.-Alanine, N-[(2R)-2,4-dihydroxy-3,3-dimethyl-1-oxobutyl]-

.beta.-Alanine, N-(2R)-2,4-dihydroxy-3,3-dimethyl-1-oxobutyl-: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

Calcium pantothenate, calcium chloride double salt is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient. /Calcium pantothenate, calcium chloride double salt/

Substance added directly to human food affirmed as generally recognized as safe (GRAS). /Calcium pantothenate/

Drug products containing certain active ingredients offered over-the-counter (OTC) for certain uses. A number of active ingredients have been present in OTC drug products for various uses, as described below. However, based on evidence currently available, there are inadequate data to establish general recognition of the safety and effectiveness of these ingredients for the specified uses: pantothenic acid is included in weight control drug products.

Sodium pantothenate used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice. /Sodium pantothenate/

NAS, Food and Nutrition Board, Institute of Medicine; Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academy Press, Washington, D.C. (1998).[Available from, as of March 2, 2010: http://www.nap.edu/catalog/6015.html]

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Although the clinical importance has not been established, the miotic effects of anticholinesterase ophthalmic preparations (eg, echothiophate iodide (no longer commercially available in the US), isoflurophate) reportedly may be potentiated by pantothenic acid.

The hypolipidemic effects of pantothenic acid derivatives (phosphopantothenate, panthenol and pantethine) were studied in mice with hypothalamic obesity ... induced by single injection of aurothioglucose (300 mg/kg body wt, ip). All the tested substances were administered during the last 10 days before decapitation (im, of dosage equivalent to 150 mg/kg body wt of phosphopantothenate). The studied substances inhibited the weight gain of the animals with hypothalamic obesity over the last 10 days of the experiment. The treatment with aurothioglucose increased food intake and mean body weight, blood glucose level; insulin, serum total cholesterol, triglyceride, the sum of LDL + VLDL and LDL-cholesterol concentration; triglyceride and cholesterol fractions in the liver; triglyceride and FFA content as well as lipoprotein lipase activity in adipose tissue of experimental mice. The administration of the assay compounds lowered food intake and mean body weight, insulin and glucose levels and decreased the content of triglycerides, total cholesterol and cholesterol esters in serum and adipose tissue as well as raised the activity of lipoprotein lipase in adipose tissue and serum lipolytic activity in obese mice. Among the compounds studied the reverse effect of panthenol was especially pronounced. The mechanism of hypolipidemic effects of pantothenic acid derivatives can be related to the reduced resistance to insulin and activation of lipolysis in serum and adipose tissue. /Panthenol, Phosphopantothenate, Pantethine/

A combination of 1.2 g of calcium pantothenate, 0.6 g of pyridoxine, 3 g of niacinamide, and 3 g of ascorbic acid taken daily for 6 weeks was associated with elevations in serum transaminase levels in children. One of these doses or the combination may therefore cause hepatotoxicity, but it is not possible from this study alone to ascribe to pantothenic acid the reported adverse effect in liver function.

... Pregnant CD-1 mice were administered a teratogenic dose of valproic acid (VPA) prior to neural tube closure and embryonic protein levels were analyzed. ... VPA (400 mg/kg)-induced NTDs (24%) and VPA-exposed embryos with a neural tube defect (NTD) showed a 2-fold increase in p53, and 4-fold decreases in NF-kappaB, Pim-1, and c-Myb protein levels compared to their phenotypically normal littermates (P<0.05). Additionally, VPA increased the ratio of embryonic Bax/Bcl-2 protein levels (P<0.05). Pretreatment of pregnant dams with either folic acid or pantothenic acid prior to VPA significantly protected against VPA-induced NTDs (P<0.05). Folic acid also reduced VPA-induced alterations in p53, NF-kappaB, Pim-1, c-Myb, and Bax/Bcl-2 protein levels, while pantothenic acid prevented VPA-induced alterations in NF-kappaB, Pim-1, and c-Myb...

For more Interactions (Complete) data for D-Pantothenic Acid (6 total), please visit the HSDB record page.

As previously stated, vitamin B5 is considered generally safe. There are no established upper limits since there have been no reports of vitamin B5 toxicity in humans with high intakes. However, there are still side effects involved with the administration of this drug, which include the following.；Common Adverse Effects；* Muscle pain；* Joint pain；* Diabetes mellitus, new-onset；* Sore throat；* Headache；* Weakness/lack of energy；* Dizziness；* Creatine phosphokinase (CPK) elevation；* Nausea；* Abdominal pain；* Alanine transaminase (ALT) elevation；* Constipation；* Flulike illness；* Urinary tract infection (UTI)；* Hypersensitivity reactions (including rash, itching, hives, and swelling)；* Pancreatitis；Less Common Adverse Effects；* Yellowing skin and eyes (jaundice)

Pantothenic acid is excreted in human breast milk with concentration directly proportional to intake. With a dietary intake of 8-15 mg/day, mean milk concentration avg 1.93-2.35 mg/mL. In a group of mothers who had delivered premature babies (26-34 weeks gestational age), pantothenic acid milk levels were significantly > a comparable group with term babies (39-41 weeks). Milk levels in the preterm group avg 3.91 mg/mL up to 40 weeks gestational age and then fell to 3.16 mg/mL. For the term group levels at 2 and 12 weeks postpartum were 2.57 and 2.55 mg/mL, respectively. A 1983 English study measured pantothenic acid levels in pooled human milk obtained from preterm (26 mothers - 29-34 weeks) and term (35 mothers - 39 weeks or longer) patients. Preterm mild rose from 1.29 mg/mL (colostrum) to 2.27 mg/mL (16-196 days), while term milk increased over the same period from 1.26 to 2.61 mg/mL.

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

Toxicity is likely at 10,000 mg daily and causes upset stomach and diarrhea as the most common symptoms, according to the National Institutes of Health (NIH) Office of Dietary Supplements.

Occurs everywhere in animal and plant tissue. The richest common source is liver, but jelly of the queen bee contains 6 times as much as liver. Rice bran and molasses are other good sources.

Liver, kidney, yeast, crude molasses, milk, whole-grain cereals, rice

Human milk contains about 2 mg/L; cow's milk, about 3.5 mg/L. Liver and other organ meats and eggs are particularly good sources. Broccoli, cauliflower, white and sweet potatoes, tomatoes and molasses are quite high in pantothenic acid. Muscle tissue of beef, pork, lamb, and chicken are also good sources.

/HUMAN EXPOSURE STUDIES/ Whether high-dose oral contraceptive agents affected pantothenic acid metabolism /was investigated/ in 13 women between the ages of 19 and 24 years enrolled in a 12-day confined study. At the end of the study, blood levels and urinary pantothenic acid excretion were similar in the subjects and controls. The investigators concluded that high-dose oral contraceptive agents do not cause significant changes in the biochemical parameters of pantothenic acid.

/HUMAN EXPOSURE STUDIES/ The aim of this study was to determine the association between dietary intake, determined using a food frequency questionnaire, and genome damage in lymphocytes measured using the micronucleus (MN) assay. The study, performed on 190 healthy individuals (mean age 47.8 years, 46% males), also examined whether a supplementation with beta-carotene, vitamins C and E along with zinc (ACEZn), in a randomized trial for 6 months, improves genome stability. Multivariate analysis of baseline data showed that (1) the highest tertile of intake of vitamin E, retinol, folic acid, nicotinic acid (preformed) and calcium is associated with significant reductions in MN frequency, i.e. -28, -31, -33, -46 and -49%, respectively (P < 0.005) relative to the lowest tertile of intake and (2) the highest tertile of intake of riboflavin, pantothenic acid and biotin was associated with significant increases in MN frequency, ie +36% (P = 0.054), +51% (P = 0.021), and +65% (P = 0.001), respectively, relative to the lowest tertile of intake. Mid-tertile beta-carotene intake was associated with an 18% reduction in MN frequency (P = 0.038); however, the highest tertile of intake (>6400 ug/day) resulted in an 18% increment in MN frequency. Supplementation with ACEZn significantly reduced the MN index by 13% (P = 0.038). The study also showed interactive additive effects such as the protective effect of increased calcium intake (-46%) and the exacerbating effect of riboflavin (+42%) on increased genome damage caused by low folate intake. The results from this study illustrate the strong impact of a wide variety of micronutrients and their interactions on genome health, depending on the level of intake.

/HUMAN EXPOSURE STUDIES/ The purpose of this study was to investigate the physiological and performance responses to supplementation with allithiamin and pantethine. On two separate occasions, six highly trained cyclists [maximum O2 consumption or VO2max 61.8 (2.1) mL/kg/min] performed a 50-km steady-state ride on a cycle ergometer at a workload corresponding to approximately 60% of VO2max followed by a 2000-m time trial. For 7 days prior to each ride, subjects daily ingested either a placebo (PL) or a combination of 1 g of allithiamin and 1.8 g of a 55%/45% pantethine/pantothenic acid compound (AP). Treatments were administered using a randomized, double-blind, counter-balanced design. During the 50 km ride, measures of heart rate, respiratory gas exchange and ratings of perceived exertion were recorded at 5, 15, 25, 35 and 45 km. Blood samples were collected at 10, 20, 30, 40 and 50 km and analyzed for lactate, glucose and free fatty acids. Blood samples for the analysis of lactate were also collected 3 and 5 min after the completion of the 2000-m time trial. There were no significant differences in any of the measured parameters between experimental conditions. Time to complete the 2000-m time trial was also not significantly different between experimental conditions [PL 178.2 (8.4), AP 170.7 (10.2) s; P=0.58]. These results suggest that, despite the reported enhanced absorption properties, supplementation with allithiamin and pantethine does not alter exercise metabolism or exercise performance.

/CASE REPORTS/ ... A 76-year-old white woman was admitted to the hospital because of chest pain and dyspnea related to pleurisy and a pericardial tamponade. This patient had no history of allergy and had been taking vitamin B5 and vitamin H for two months. Blood tests performed showed an inflammatory syndrome and a high eosinophil concentration (1200-1500 cells/cu mm). Pleurocentesis and pericardiotomy yielded a sterile exudative fluid with an eosinophilic infiltrate. There were no nuclear antibodies and no rheumatic factor; screenings for viruses, parasites, bacteria, and malignant tumor were negative. A myelogram, biopsy of the iliac crest bone, and concentration of immunoglobulin E were also normal. After withdrawal of the vitamins, the patient recovered and the eosinophilia disappeared. ... This case suggests that vitamin B5 and vitamin H may cause symptomatic, life-threatening, eosinophilic pleuropericarditis. Physicians prescribing these commonly used vitamins should be aware of this potential adverse reaction.

For more Human Toxicity Excerpts (Complete) data for D-Pantothenic Acid (7 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Male rats at 21 d of age were given 0.03% pantothenic acid in their drinking water for 9 weeks. After 9 weeks of treatment, the animals were decapitated, and adrenal cells were cultured in the absence or presence of rat adrenocorticotropic hormone (ACTH; 10-15 to 10-10 M) and/or ovine prolactin (oPRL; 10-9 to 10-7 M) for 4 hr. Adrenal cells in pantothenic acid-treated rats exhibited higher basal levels of corticosterone and progesterone than control rats. The response of ACTH and/or PRL on corticosterone and progesterone release was higher in the pantothenic acid-treated rats than in the control rats. In addition, PRL increased the stimulatory effect of ACTH-induced corticosterone secretion in both normal and pantothenic acid-treated rats. These results clearly demonstrated that pantothenic acid supplementation stimulates the ability of adrenal cells in male rats to secrete corticosterone and progesterone. Additionally, these results also showed that pantothenic acid supplementation induced adrenal hyperresponsiveness to ACTH stimulation, and PRL further stimulated adrenal sensitivity to ACTH.

/OTHER TOXICITY INFORMATION/ Pantothenic acid exhibits no outstanding pharmacodynamic actions following administration to experimental animals ...

NIOSH (NOES Survey 1981-1983) has statistically estimated that 4,854 workers (52 of these were female) were potentially exposed to d-pantothenic acid in the US(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 197 workers (52 of these were female) were potentially exposed to sodium pantothenate in the US(1). /Sodium pantothenate/

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Chemical: .beta.-Alanine, N-[(2R)-2,4-dihydroxy-3,3-dimethyl-1-oxobutyl]-

.beta.-Alanine, N-(2R)-2,4-dihydroxy-3,3-dimethyl-1-oxobutyl-: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

Calcium pantothenate, calcium chloride double salt is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient. /Calcium pantothenate, calcium chloride double salt/

Substance added directly to human food affirmed as generally recognized as safe (GRAS). /Calcium pantothenate/

Drug products containing certain active ingredients offered over-the-counter (OTC) for certain uses. A number of active ingredients have been present in OTC drug products for various uses, as described below. However, based on evidence currently available, there are inadequate data to establish general recognition of the safety and effectiveness of these ingredients for the specified uses: pantothenic acid is included in weight control drug products.

Sodium pantothenate used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice. /Sodium pantothenate/

Pantothenic acid is vital to the synthesis and maintenance of coenzyme A (CoA), a cofactor and acyl group carrier for many enzymatic processes, and acyl carrier protein, a component of the fatty acid synthase complex. As such, pantothenic acid is essential to almost all forms of life. Most tissues transport pantothenic acid into cells for the synthesis of CoA. CoA, in forms such as acetyl CoA and succinyl CoA, plays an important role in the tricarboxylic acid cycle and in the synthesis of fatty acids and membrane phospholipids, amino acids, steroid hormones, vitamins A and D, porphyrin and corrin rings, and neurotransmitters. It is also required for the acetylation and acylation of proteins and the synthesis of alpha-tubulin.

Pantothenic acid functions as a component of coenzyme A (CoA), which is involved in fatty acid metabolism. Pantothenic acid is widely distributed in foods and is essential to almost all forms of life ... Adequate Intake (AIs) for pantothenic acid are based on pantothenic acid intake sufficient to replace urinary excretion ... DRI values are listed by life stage group in the table.；Table: Dietary Reference Intakes for Pantothenic Acid by Life Stage Group (mg/day) [Table#2688]

... Pantothenic acid, pantothenol and other derivatives ... are precursors of CoA /that/ protect cells and whole organs against peroxidative damage by increasing the content of cell glutathione...

A member of the B complex vitamins; essential vitamin for the biosynthesis of coenzyme A in mammalian cells. Occurs ubiquitously in all animal and plant tissue.

For more Bionecessity (Complete) data for D-Pantothenic Acid (24 total), please visit the HSDB record page.

Pantothenic acid is used in the synthesis of coenzyme A (CoA). CoA is thought to act as a carrier molecule, allowing the entry of acyl groups into cells. This is of critical importance as these acyl groups are used as substrates in the tricarboxylic acid cycle to generate energy and in the synthesis of fatty acids, cholesterol, and acetylcholine. Additionally, CoA is part of acyl carrier protein (ACP), which is required in the synthesis of fatty acids in addition to CoAs use as a substrate. Pantothenic acid in the form of CoA is also required for acylation and acetylation, which, for example, are involved in signal transduction and enzyme activation and deactivation, respectively. Since pantothenic acid participates in a wide array of key biological roles, it may have numerous wide-ranging effects.

Pantothenic acid is incorporated into COENZYME A and protects cells against peroxidative damage by increasing the level of GLUTATHIONE.

... To test the functional effect of pantothenate on dermal fibroblasts, cells were cultured and in vitro proliferation tests were performed using a standardized scratch test procedure. For all three donors analyzed, a strong stimulatory effect of pantothenate at a concentration of 20 ug/mL on the proliferation of cultivated dermal fibroblasts was observed. To study the molecular mechanisms resulting in the proliferative effect of pantothenate, gene expression was analyzed in dermal fibroblasts cultivated with 20 ug/mL of pantothenate compared with untreated cells using the GeneChip Human Exon 1.0 ST Array. A number of significantly regulated genes were identified including genes coding for interleukin (IL)-6, IL-8, Id1, HMOX-1, HspB7, CYP1B1 and MARCH-II. Regulation of these genes was subsequently verified by quantitative real-time polymerase chain reaction analysis. Induction of HMOX-1 expression by pantothenol and pantothenic acid in dermal cells was confirmed on the protein level using immunoblots. Functional studies revealed the enhanced suppression of free radical formation in skin fibroblasts cultured with panthenol. In conclusion, these studies provided new insight in the molecular mechanisms linked to the stimulatory effect of pantothenate and panthenol on the proliferation of dermal fibroblasts. /Calcium pantotenate/

Coenzyme A (CoA) is the major acyl group carrier in intermediary metabolism. Hopantenate (HoPan), a competitive inhibitor of the pantothenate kinases, was used to chemically antagonize CoA biosynthesis. HoPan dramatically reduced liver CoA and mice developed severe hypoglycemia. Insulin was reduced, glucagon and corticosterone were elevated, and fasting accelerated hypoglycemia. Metabolic profiling revealed a large increase in acylcarnitines, illustrating the role of carnitine in buffering acyl groups to maintain the nonesterified CoASH level. HoPan triggered significant changes in hepatic gene expression that substantially increased the thioesterases, which liberate CoASH from acyl-CoA, and increased pyruvate dehydrogenase kinase 1, which prevents the conversion of CoASH to acetyl-CoA. These results identify the metabolic rearrangements that maintain the CoASH pool which is critical to mitochondrial functions, including gluconeogenesis, fatty acid oxidation, and the tricarboxylic acid and urea cycles.

The synthesis of Coenzyme A (CoA) from pantothenate is regulated primarily by pantothenate kinase, an enzyme that is inhibited by the pathway end products, CoA and acyl CoA.

/P/antothenic acid is required for intermediary metabolism of carbohydrates, proteins, and lipids. Pantothenic acid is a precursor of coenzyme A which is required for acetylation (acyl group activation) reactions in gluconeogenesis, in the release of energy from carbohydrates, the synthesis and degradation of fatty acids, and the synthesis of sterols and steroid hormones, porphyrins, acetylcholine, and other compounds.

Absorption Coenzyme A (CoA). CoA in the diet is hydrolyzed in the intestinal lumen to dephospho CoA, phosphopantetheine, and pantetheine, with the pantetheine subsequently hydrolyzed to pantothenic acid. Pantothenic acid was the only one of these pantothenate-containing compounds absorbed by rats in studies on absorption of the various forms. Absorption is by active transport at low concentrations of the vitamin and by passive transport at higher concentrations in animal models. Because the active transport system is saturable, absorption will be less efficient at higher concentrations of intake, but the intake levels at which absorptive efficiency decreases in humans are not known.

Intestinal microflora have been observed to synthesize pantothenic acid in mice, but the contribution of bacterial synthesis to body pantothenic acid levels or fecal losses in humans has not been quantified. If microbial synthesis is substantial, balance studies in humans may have underestimated pantothenic acid absorption and requirements.

Coenzyme A (CoA) is hydrolyzed to pantothenate in a multiple-step reaction. The pantothenic acid is excreted intact in urine, ... . The amount excreted varies proportionally with dietary intake over a discrete yet wide range of intake values.

Dietary pantothenic acid is primarily in the form of CoA or ACP and must be converted into free pantothenic acid for absorption. CoA and ACP are hydrolyzed into 4'-phosphopantetheine which is then dephosphorylated into pantetheine and subsequently hydrolyzed again to free pantothenic acid by Pantetheinase in the intestinal lumen. Free pantothenic acid is absorbed into intestinal cells via a saturable, sodium-dependent active transport system with passive diffusion acting as a secondary pathway. As intake increases up to 10-fold absorption rate can decrease to as low as 10% due to transporter saturation.

Pantothenic acid is absorbed in the small intestine by active transport at low concentrations of the vitamin and by passive transport at higher concentrations. Because the active transport system is saturable, absorption is less efficient at higher concentrations of intake. However, the exact intake levels at which absorption decreases in humans are not known. Pantothenic acid is excreted in the urine in amounts that are proportional with dietary intake over a wide range of intake values.

Pantothenic acid is readily absorbed from the GI tract. It is present in all tissues, in concentrations ranging from 2-45 ug/g. Pantothenic acid apparently is not destroyed in human body since intake and excretion ... are approximately equal. About 70% of unchanged pantothenic acid is excreted in urine and about 30% in feces.

Pantothenic acid is readily absorbed from the GI tract following oral administration. Normal serum pantothenate concentrations are 100 ug/mL or greater. /Pantothenic acid/ is widely distributed into body tissues, mainly as coenzyme A. Highest concentrations are found in the liver, adrenal glands, heart, and kidneys. Milk of nursing mothers receiving a normal diet contains about 2 ug of pantothenic acid per mL. About 70% of an oral dose of pantothenic acid is excreted unchanged in urine and about 30% in feces.

... /N/ewborn pantothenic acid levels are significantly greater than maternal levels. At term, mean pantothenate levels in 174 mothers were 430 ng/mL (range 250-710) and in their newborns 780 ng/mL (range 400-1480). Placental transfer of pantothenate to the fetus is by active transport, but it is slower than transfer of other B complex vitamins. In one report, low-birth-weight infants had significantly lower levels of pantothenic acid than did normal weight infants.

For more Absorption, Distribution and Excretion (Complete) data for D-Pantothenic Acid (20 total), please visit the HSDB record page.

CIR ingredient: Pantothenic Acid

A B complex vitamin found in all plants and animals that is essential for the biosynthesis of coenzyme A in mammals; [Merck Index] Permitted for use as an inert ingredient in non-food pesticide products; [EPA]

... Commonly included in multivitamin preparations and in products for enteral and parenteral alimentation.

Food additive /Sodium pantothenate/

BIOLOGICAL ACTIVITIES: Antiallergic; antiarthritic; antiephalagic; possible anticlaudificant; antidermatitic; antifatigue; antihypercholesterolemic; possible antiielus; possible antiinsomniac; possible antirheumatitic; cancer-preventive

THERAPEUTIC CATEGORY: Vitamin

The biosynthesis of pantothenic acid proceeds via enzyme-catalyzed condensation of pantoic acid with beta-alanine in the presence of adenosine triphosphate.

The starting materials for the large-scale production of calcium (R)-pantothenate, the commercial form of pantothenic acid, are (R)-pantolactone and calcium beta-alaninate. ... Calcium (R)-pantothenate is obtained by the reaction of calcium beta-alaninate with (R)-pantolactone in boiling methanol or ethanol. Depending on the crystallization and drying conditions, three solventless polymorphous forms, two solvates, and an amorphous product can be isolated. Hygroscopic prisms with four moles of methanol and one mole of water are formed on crystallization from 90% aqueous methanol at 0 °C. Drying of these prisms at 80 °C and 30 mbar produces X-ray amorphous calcium (R)-pantothenate while maintaining the crystal form. Calcium (R)-pantothenate can be produced by seeded crystallization in 90% aqueous methanol by exploiting the higher solubility of the racemate compared with the solvates of the enantiomers. Racemization of the S form is achieved with sodium methoxide in anhydrous methanol. /Calcium (R)-pantothenate/

Sodium (R)-pantothenate is isolated by reacting sodium beta-alaninate with (R)-pantolactone in methanol or ethanol (1 hour, 65 °C). On cooling, it crystallizes in the form of square platelets (mp 160 - 165 °C) and is highly hygroscopic. /Sodium (R)-pantothenate/

Dexpanthenol (injection): solution 250 mg/mL in 2 and 10 mL containers; pantothenic acid (oral): tablets 50, 100, and 200 mg.

Oral: Tablets: 100 mg, 200 mg, 250 mg, 500 mg.(Available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name.)

Calcium pantothenate is available as tablets containing from 10 to 545 mg

EPA Safer Chemical Functional Use Classes -> Skin Conditioning Agents

Safer Chemical Classes -> Green half-circle - The chemical is expected to be of low concern

Cosmetics -> Hair conditioning; Skin conditioning; Antistatic

Pantothenic acid is included in multiple vitamin preparations as the calcium or sodium salt or the alcohol, panthenol.

Pantothenic acid derivatives sold commercially are prepared by synthesis. May be prepared by the direct condensation of beta-alanine with the optically resolved form of the lactone of pantoic acid (2,4-dihydroxy-3,3-dimethylbutyric acid) which is prepared from isobutyraldehyde.

Panthenol is the most stable in liquid products, but is not recommended for use in foods ... D,L-calcium pantothenate-calcium chloride complex is less hygroscopic and has superior stability in multivitamin tablets ... Calcium pantothenate has good stability in dry mixes such as grain based complete protein foods.

Pantothenic acid appears to reduce the toxicity of number of drugs including antibiotics, and the pantothenate forms of aminoglycoside antibiotics have been made and used to reduce the parent drug's potential toxicity.

For more General Manufacturing Information (Complete) data for D-Pantothenic Acid (7 total), please visit the HSDB record page.