| Size | Price | |
|---|---|---|
| Other Sizes |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
In skin conditioning agents, the proportions of 5%, 10%, and 20% sodium pyridinecarboxylate absorbed through human skin have been observed to be 5.97%, 6.78%, and 5.89%, respectively. In canine animal models, it has been determined that 30% of orally absorbed pyridinecarboxylic acid is excreted unchanged in the urine, with the remainder converted to urea. Currently, there are no available data regarding the volume of distribution of pyridinecarboxylic acid. Currently, there are no available data regarding the clearance rate of pyridinecarboxylic acid. Metabolism/Metabolites In living cells, there are multiple metabolic pathways involving pyridinecarboxylic acid: (a) glutamine/glutamine (amino acid) n is converted to pyroglutamine- (amino acid) n by glutamine cyclase; (a) pyroglutamine- (amino acid) n is then metabolized to pyroglutamate (pyrrolic acid) by pyroglutamyl peptidase; (b) via the γ-glutamyl cycle, γ-glutamyl transpeptidase generates γ-glutamyl amino acids, which are then metabolized to pyroglutamate by γ-glutamyl cyclase; (c) glutamate is metabolized to γ-glutamyl phosphate by γ-glutamylcysteine synthase, glutamine synthase, or glutamate 5-kinase, which itself can be converted to pyroglutamate; (d) glutamate or glutamine can be non-enzymatically converted to pyroglutamate. Finally, pyroglutamate (or pyridinecarboxylic acid) itself is metabolized to glutamate by 5-oxoprolinease. 5-oxoproline is part of the glutathione metabolic pathway. The degradation of glutathione is initiated by gamma-glutamyl transferase, which catalyzes the transfer of the gamma-glutamyl group of glutathione to the receptor. The gamma-glutamyl residue is a substrate of gamma-glutamyl cyclotransferase, which converts it to 5-oxoproline and the corresponding amino acid. The conversion of 5-oxoproline to glutamate is catalyzed by 5-oxoprolyase. (T527) Biological Half-Life Some studies have shown that the specific half-life of N-terminal glutamate is approximately 9 months in a buffer solution at pH 4.1 and 45°C. |
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| Toxicity/Toxicokinetics |
Toxicity Summary
S-O-prolineuria occurs in patients with moderate to severe glutathione synthase deficiency. Glutathione synthase deficiency leads to the accumulation of gamma-glutamylcysteine, which is converted to s-oxoproline by gamma-glutamyl cyclotransferase. Excessive production of s-oxoproline exceeds the catalytic capacity of s-oxoproline enzyme, leading to its accumulation in body fluids, causing metabolic acidosis and s-oxoprolineuria. Accumulation of s-oxoproline is considered a cause of metabolic acidosis in Hawking's disease. s-oxoproline enzyme deficiency also reduces the conversion of s-oxoproline to glutamate, resulting in elevated s-oxoproline levels in body fluids. S-oxoprolineuria is also seen in patients with urea cycle defects, such as ornithine transcarbamate deficiency or homocysteineuria. In nephrotic cystinopathy, seroprolineuria may be due to secondary impairment of the γ-glutamyl cycle caused by reduced availability of free cysteine, which can be corrected with cysteine treatment. Transient seroprolineuria of unknown cause has been reported in extremely premature infants. Malnutrition and limited glycine availability during pregnancy, as well as increased turnover of collagen, fibrinogen, and other proteins containing high levels of seroproline in patients with severe burns or Stevens-Johnson syndrome, may contribute to seroprolineuria. Furthermore, certain medications, such as acetaminophen, vigabatrin, or some antibiotics (flucloxacillin, netilmicin), are known to induce seroprolineuria, possibly through interactions with the γ-glutamyl cycle. Some infant formulas and tomato juice may contain modified proteins with increased seroproline content. (T527) Protein Binding Currently, there is no readily available data on protein binding of pyridinecarboxylic acid. |
| Additional Infomation |
Pharmacodynamics
Pyridinecarboxylic acid is a naturally occurring but poorly studied amino acid derivative that can be produced via enzymatic or non-enzymatic pathways and participates in various chemical pathways as a biological intermediate. Elevated levels of pyridinecarboxylic acid in the blood may be associated with abnormal glutamine or glutathione metabolism. Pyridinecarboxylic acid is usually present in large quantities in the brain and other tissues (such as skin) in its bound form. Furthermore, high concentrations of pyridinecarboxylic acid can induce acidosis as an acid-producing agent and cause adverse health effects as a metabolic toxin. Long-term elevated levels of pyridinecarboxylic acid are associated with at least five congenital metabolic defects, including seroprolineuria (where seroproline is also known as pyridinecarboxylic acid), seroprolinease deficiency, glutathione synthase deficiency, Hodgkin's urine disease, and propionic acidemia. Specifically, abnormally elevated levels of organic acids such as pyridinecarboxylic acid in the blood, urine, brain tissue, and/or other tissues can lead to systemic metabolic acidosis. This acidosis typically occurs when the arterial blood pH is below 7.35. Early symptoms of infantile acidosis include feeding difficulties, vomiting, loss of appetite, hypotonia, and lethargy. Ultimately, acidosis and its symptoms can lead to heart, liver, and kidney abnormalities, seizures, coma, and even death. Many children with organic acidemia experience intellectual disability or developmental delays. In adults, acidosis or acidosis is characterized by headache, confusion, fatigue, tremors, drowsiness, and seizures. An overdose of acetaminophen can also cause elevated levels of pyridinecarboxylic acid in the blood, leading to increased acidity, a condition known as hyperanion gap metabolic acidosis. |
| Molecular Formula |
C5H7NO3
|
|---|---|
| Molecular Weight |
129.11
|
| Exact Mass |
129.042
|
| CAS # |
98-79-3
|
| PubChem CID |
7405
|
| Appearance |
White to light yellow solid powder
|
| Density |
1.6±0.1 g/cm3
|
| Boiling Point |
382.4±52.0 °C at 760 mmHg
|
| Melting Point |
160-163 °C(lit.)
|
| Flash Point |
185.1±30.7 °C
|
| Vapour Pressure |
0.0±2.0 mmHg at 25°C
|
| Index of Refraction |
1.627
|
| LogP |
-1.95
|
| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
3
|
| Rotatable Bond Count |
1
|
| Heavy Atom Count |
9
|
| Complexity |
154
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
C1CC(=O)N[C@@H]1C(=O)O
|
| InChi Key |
ODHCTXKNWHHXJC-VKHMYHEASA-N
|
| InChi Code |
InChI=1S/C5H7NO3/c7-4-2-1-3(6-4)5(8)9/h3H,1-2H2,(H,6,7)(H,8,9)/t3-/m0/s1
|
| Chemical Name |
(2S)-5-oxopyrrolidine-2-carboxylic acid
|
| Synonyms |
EINECS 202-700-3; Glutimic acid; Pidolic acid; NSC-9966; NSC143034; NSC 9966; NSC9966;
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~774.53 mM)
H2O : ~100 mg/mL (~774.53 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (19.36 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (19.36 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (19.36 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 140 mg/mL (1084.35 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 7.7453 mL | 38.7267 mL | 77.4533 mL | |
| 5 mM | 1.5491 mL | 7.7453 mL | 15.4907 mL | |
| 10 mM | 0.7745 mL | 3.8727 mL | 7.7453 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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