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HCID 449Erstellt: 30. Oktober 2026

Mevalonic Acid

Mevalonic acid · MVS · MK 91 · (±)-MVA-Li · rac.-MVA-Li · Hiochic Acid · RS-Mevalonic Acid · D,L-Mevalonic Acid

https://huagongshe.com/de/chemical/449

Molekülstruktur von Mevalonic Acid

Identifikatoren & physikalische Daten

CAS No.150-97-0
SummenformelC6H12O4
Durchschnittliche Molmasse148,16 g/mol
Monoisotopische Masse148,07355886 g/mol
SMILESCC(O)(CCO)CC(=O)O
InChIKeyKJTLQQUUPVSXIM-UHFFFAOYSA-N
PubChem CID449
ChEMBLCHEMBL1794734
ChEBICHEBI:25351
DTXSIDDTXSID5040546

Chemische & physikalische Eigenschaften

XLogP-1
Polarare Oberfläche (TPSA)77,8
H-Brücken-Donoren3
H-Brücken-Akzeptoren4
Frei drehbare Bindungen4
Schwere Atome10
Formalladung0
Komplexität123
Color/FormOily liquid
LöslichkeitVery soluble in water, but also soluble in organic solvents, especially polar organic solvents.Soluble in DMSO
Optical RotationCrystals from benzene + petroleum ether, mp 96-97 °C. Specific optical rotation: -20 deg at 20 °C/D (c = 2 in ethanol) /Benzhydrylamide/
Other Experimental PropertiesHygroscopic crystals, mp 28 °C /delta-Lactone/
Lagerbedingungen2-8°C
AggregatzustandSolid
Siedepunkt364.1±32.0 °C(Predicted)
Dichte1.263±0.06 g/cm3(Predicted)
Schmelzpunkt151-152 °C(Solv: benzene (71-43-2))
pKa (Säurekonstante)4.33±0.10(Predicted)
FarbeWhite to off-white
Specific Activity10-20 Ci/mmol
InChI1S/C6H12O4/c1-6(10,2-3-7)4-5(8)9/h7,10H,2-4H2,1H3,(H,8,9)
InChIKeyKJTLQQUUPVSXIM-UHFFFAOYSA-N
SMILESOC(CCO)(CC(=O)O)C
EPA chemische InformationenPentanoic acid, 3,5-dihydroxy-3-methyl- (150-97-0)

Sicherheit & Vorschriften

EntsorgungsverfahrenSRP: At the time of review, 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.
Wechselwirkungen... The effect of topical mevalonic acid on the murine epidermal permeability barrier function /was investigated/, comparing it with that of cholesterol. Topical treatment with acetone caused linear increases in transepidermal water loss, in proportion to the number of treatments more rapidly in aged mice than in young mice. Administration of mevalonic acid on aged murine epidermis enhanced its resistance against damage and the recovery rate of barrier function from acute barrier disruption. In contrast, although cholesterol also had the same effect, it required a much higher amount than mevalonic acid. In young mice, neither mevalonic acid nor cholesterol had any effect on resistance against acetone damage nor the recovery rate from acetone damage. In the skin of mice topically administered with mevalonic acid, stimulation of cholesterol synthesis and 3-hydroxy-3-methylglutaryl coenzyme A reductase activity were both observed, whereas none was seen with stimulation by equimolar cholesterol. These data indicate that a topical application of mevalonic acid enhances barrier recovery in aged mice, which is accompanied by not only acceleration of cholesterol synthesis from mevalonic acid but also stimulation of the whole cholesterol biosynthesis.The influence of 2 different alcoholic beverages containing an equal amount of alcohol (48 g), 1 with mevalonic acid (beer) and 1 without (vodka), on the urinary excretion and serum concentration of mevalonic acid was investigated in 7 healthy subjects. Drinking 1 L of beer at night containing 608 ug/L mevalonic acid more than doubled the urinary excretion of mevalonic acid the following 12 hours, on average from 103 +/- 15 microg/12 h to 211 +/- 17 ug/12 hr (P < .00118% of the administered dose). Drinking the same amount of alcohol as vodka had no effect, but urinary mevalonic acid output increased slightly the following day (7 AM to 7 PM) after ingestion of both alcoholic beverages. Serum concentrations of mevalonic acid were significantly increased the following morning after ingestion of beer (from 3.22 +/- 0.20 ng/mL to 6.79 +/- 0.58 ng/mL) or vodka (from 3.23 +/- 0.37 ng/mL to 5.36 +/- 0.55 ng/mL, P < .002 for both). An increase in the ratio of lathosterol to cholesterol in serum, another indicator of 3beta-hydroxy-3beta-methylglutaryl coenzyme A reductase activity in the liver, was also observed (+18% and +25%, respectively). ... Studies using mevalonic acid as a marker of cholesterol synthesis must be carefully monitored regarding dietary mevalonic acid intake and alcohol consumption.

Anwendungen & Verwendung

Verwenden

Precursor in the biosynthesis of cholesterol. Occurs in equilibrium with the d-lactone

Mevalonic acid is a product of the enzyme HMG-CoA reductase which is essential for cholesterol biosynthesis. Fluvastatin (Sandoz compound XU 62-320) is a potent inhibitor of this enzyme and, hence, mevalonic acid production. In three separate studies, oral administration of fluvastatin at 12 and 24 mg/kg/day to mated rats from day 15 of gestation through weaning resulted in unanticipated maternal mortality at the time of parturition and during lactation. Microscopic evaluations performed in two studies revealed significant cardiac myopathy in the dying animals. Drug-related clinical signs, significant maternal body weight loss, and an increase in stillborn pups and neonatal mortality were also noted at one or both dose levels. Supplementation of fluvastatin administration with 500 mg/kg b.i.d. of mevalonic acid completely blocked and/or ameliorated the mortality, cardiac myopathy, and other adverse effects. These studies indicate that the adverse maternal effects observed with fluvastatin before or following parturition resulted from exaggerated pharmacologic activity at the dose levels administered, i.e., inhibition of the enzyme HMG-CoA reductase, its immediate product mevalonic acid, and cholesterol biosynthesis.
... Mevalonic acid prevented the inhibitory effect of atorvastatin on cytokine-stimulated vascular cell adhesion molecule-1 expression and subsequent adhesion of THP-1 monocytes to the cultured endothelial cells.
Human Toxicity Excerpts/SIGNS AND SYMPTOMS/ Defects of cholesterol biosynthesis comprise a heterogeneous group of disorders... . Mevalonic aciduria (MVA) and hyperimmunoglobulinemia D syndrome (HIDS) are due to allelic defects in mevalonate kinase, an enzyme located proximally in the pathway of cholesterol and nonsterol isoprene biosynthesis. Clinically, patients affected with these disorders present with recurrent febrile attacks. This is the only manifestation in most patients with HIDS, and, in the case of classical mevalonic aciduria, is part of a severe multisystemic disease, including malformations, severe failure to thrive and neurological abnormalities. ... The diagnosis of MVA and HIDS is based on determination of mevalonic acid in urine followed by determination of enzyme activity.../SIGNS AND SYMPTOMS/ The febrile crises /in mevalonate kinase deficiency/ are similar to those observed in hyperimmunoglobulinemia D and periodic fever syndrome (HIDS). Pathogenic mutations in the mevalonate kinase gene in both disorders have demonstrated a common genetic basis./CASE REPORTS/ Mevalonic aciduria is a rare disease that is a consequence of a deficiency of mevalonate kinase, an inborn error in the biosynthesis of cholesterol. Approximately 30 cases have been reported. ... Data on two siblings with mevalonic aciduria /are contributed/ to the recognition of this subject. Both were born after uneventful pregnancies. Their parents were healthy and not consanguineous. They had normal somatic and psychomotor development until they were around 2 years old. After the second year of life they developed mental retardation, ataxia and hypotonia. MRI showed cerebellar atrophy of both hemispheres and vermis. One sibling, from the age of 10 years onwards, suffered from complex partial seizures that were controlled with levetiracetam and lamotrigine. At 11 and 12 years of age, respectively, they were able to walk without help, but their gait was broad and ataxic. Their speech was dysarthric, fine motor skills were impaired as result of cerebellar ataxia, and they had moderate mental retardation. Diagnosis of mevalonic aciduria was made at this age through urinary organic acid analysis by gas chromatography-mass spectroscopy, which revealed high urinary excretion of mevalonic acid. They are currently 18 and 17 years old, respectively, show mental retardation and are able to walk but with difficulty. In our patients, ataxia due to cerebellar atrophy and mental retardation have been the predominant clinical manifestations. In mildly affected patients who survive infancy, these seem to be the predominant findings./CASE REPORTS/ The analysis of amniotic fluids of two pregnancies at risk for mevalonic aciduria showed a 3277-fold elevation as compared to controls in the first case, diagnostic of an affected fetus, and a normal value in the second one. Mevalonic acid concentration was much increased in tissues of the affected and aborted fetus. Concentrations ranged from 840 to 1120 mumol/kg in various tissues and were as high as 1810 umol/kg in brain. Concentrations in control fetal tissues were approximately 1 umol/kg.For more Human Toxicity Excerpts (Complete) data for MEVALONIC ACID (7 total), please visit the HSDB record page.
Antidote and Emergency Treatment/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/
Wassergefährdungsklasse (WGK)3
Lagerklasse11 - Combustible Solids
Gefahrstoffdaten150-97-0(Hazardous Substances Data)