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Purity: ≥98%
Folic acid (also known as Vitamin M; Vitamin B9; folate) is a one of the B vitamins and is necessary for the production and maintenance of new cells, for DNA synthesis and RNA synthesis. The synthesis of DNA, RNA, and the metabolism of amino acids—which are necessary for cell division—require folate, which is found in different forms as folic acid, folacin, and vitamin B9. Folate is a necessary vitamin because humans cannot produce it; therefore, it must come from food. Intake of 400 micrograms of folate per day from food or dietary supplements is advised for adults in the United States.
| Targets |
Human Endogenous Metabolite; Microbial Metabolite
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|---|---|
| ln Vitro |
Folic acid treatment increases the expression of BRCA1 mRNA in HepG2, Huh-7D12, Hs578T, and JURKAT cells and BRCA2 mRNA in HepG2, Hs578T, MCF7, and MDA-MB-157 cells in a dose-dependent manner. FA has no effect on any of the ovarian cell lines or the corresponding normal cells. In Hs578T cells, folic acid increases BRCA1 protein expression but not HepG2 cell expression; BRCA2 protein expression is not detected. While there are short-term effects on breast-derived cells, FA treatment has no effect on DNA repair in liver-derived cells. FA treatment has no effect on the methylation of the BRCA1 or BRCA2 DNA, however some cell lines have different levels of methylation at particular CpG loci[1].
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| ln Vivo |
No folic acid (1, 5 mg/kg; interface) prevents epigenetic modifications of gene expression in chromosomal offspring in mice adapted to a new environment [3]. Folic acid (10, 50, 100 mg/kg; side) exhibits antidepressant-like effects in this behavioral mouse model [2].
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| Cell Assay |
All cell lines were treated with 0, 25, 50, 75, or 100 nmol/L FA for 72 hours prior to harvesting in TRI Reagent in accordance with the manufacturer's instructions in order to ascertain the impact of FA supplementation on BRCA1 and BRCA2 mRNA expression.
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| Animal Protocol |
Animal/Disease Models: 30-40 g Swiss mice [2]
Doses: 10, 50, 100 mg/kg Route of Administration: Oral Experimental Results: diminished immobility time in the forced swim test (FST) (F324=11.21), and Immobility time in the tail suspension test (TST) had a significant effect (F3, 20=5.71). Animal/Disease Models: 30-40 g Swiss mice [2] Doses: 1-10 nmol/site Route of Administration: Intracerebroventricular injection Experimental Results: diminished mouse FST (F3,22=12.31) and TST (F3,22=5.50) immobile time). Animal/Disease Models: Virgin female Wistar rats [3] Doses: 1, 5 mg/kg (180 g/kg protein plus 1 mg/kg folic acid or 90 g/kg casein plus 1, 5 mg/kg folic acid) Route of Administration: Oral administration Experimental Results: Prevention of epigenetic modifications in liver gene expression in offspring. |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Folic acid is absorbed rapidly from the small intestine, primarily from the proximal portion. Naturally occurring conjugated folates are reduced enzymatically to folic acid in the gastrointestinal tract prior to absorption. Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour. After a single oral dose of 100 mcg of folic acid in a limited number of normal adults, only a trace amount of the drug appeared in the urine. An oral dose of 5 mg in 1 study and a dose of 40 mcg/kg of body weight in another study resulted in approximately 50% of the dose appearing in the urine. After a single oral dose of 15 mg, up to 90% of the dose was recovered in the urine. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Small amounts of orally administered folic acid have also been recovered in the feces. Folic acid is also excreted in the milk of lactating mothers. Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver. Folic acid is absorbed rapidly from the GI tract following oral administration oral administration; the vitamin is absorbed mainly in the proximal portion of the small intestine. The monoglutamate forms of folate, including folic acid, are transported across the proximal small intestine via a saturable pH-dependent process. Higher doses of the pteroylmonoglutamates, including folic acid, are absorbed via a nonsaturable passive diffusion process. The efficiency of absorption of the pteroylmonoglutamates is greater than that of pteroylpolyglutamates. Following oral administration, peak folate activity in blood occurs within 30 to 60 minutes. Synthetic folate is almost 100% bioavailable when administered in fasting individuals. While the bioavailability of naturally occurring folate in food is about 50%, bioavailability of synthetic folic acid consumed with a meal ranges from 85 to 100%. Approximately two-thirds of folate in plasma is protein bound. ... When pharmacologic doses of folic acid are administered, a significant amount of unchanged folic acid is found in the plasma. The liver contains more than 50% of the body stores of folate, or about 6 to 14 milligrams. The total body store of folate is about 12 to 28 miligrams. For more Absorption, Distribution and Excretion (Complete) data for FOLIC ACID (11 total), please visit the HSDB record page. Metabolism / Metabolites Folic acid is metabolized in the liver into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF) by the enzyme dihydrofolate reductase (DHFR). Folic acid is converted (in the presence of ascorbic acid) in the liver and plasma to its metabolically active form (tetrahydrofolic acid) by dihydrofolate reductase. Following absorption of 1 mg or less, folic acid is largely reduced and methylated in the liver to N-methyltetrahydrofolic acid... . The folates are taken up by the liver and metabolized to polyglutamate derivatives (principally pteroylpentaglutamate), via the action of folypolyglutamate synthase. ... Folate polyglutamates are released from the liver to the systemic circulation and to the bile. When released from the liver into the circulation, the polyglutamate forms are hydrolyzed by gamma-glutamylhydrolase and reconverted to the monoglutamate forms. |
| Toxicity/Toxicokinetics |
Toxicity Summary
IDENTIFICATION: Folic acid is an antianaemic vitamin. Origin of the substance: Folic acid was isolated from green leafy vegetables, liver, yeast and fruits. Synthetic folic acid is commercially available. Yellow to orange brown crystalline powder which is odorless. Readily soluble in alkali, hydroxides and carbonates. Insoluble in alcohol, acetone, chloroform and ether. Solutions are inactivated by ultraviolet light. Alkaline solutions are sensitive to oxidation and acid solutions are sensitive to heat. Indications: For the prevention and treatment of vitamin B deficiency. For the treatment of megaloblastic anemia and macrocytic anemia due to folic acid deficiency. Folic acid supplements may be required in low birth weight infants, infants breastfed by folic acid deficient mothers, or those with prolonged diarrhea and infection. Other conditions which may increase folic acid requirements include alcoholism, hepatic disease, hemolytic anemia, lactation, oral contraceptive use and pregnancy. It has been given to pregnant mothers to reduce the risk of birth defects. HUMAN EXPOSURE: Main risks and target organs: Folic acid is relatively non-toxic. However, there have been reports of reactions to parenteral injections. Allergic reactions to folic acid have been rarely reported. Summary of clinical effects: Severe allergic reactions are characterized by hypotension, shock, bronchospasm, nausea, vomiting, rash, erythema. Itching may also occur. Adverse gastrointestinal and central nervous system effects have been reported. Treatment with folic acid is usually well tolerated except for rare reports of allergic reactions. Bioavailability: Folic acid is rapidly absorbed from gastrointestinal tract following oral administration. Peak folate activity in blood is 30 to 60 minutes after oral administration. Contraindications: It should be given with caution to patients with abnormal renal function. It is also contra-indicated in patients who show hypersensitivity reactions to folic acid. Caution is advised in patients who may have folate dependent tumours. Folic acid should never be given alone or in conjunction with inadequate amounts of Vitamin B12 for the treatment of undiagnosed megaloblastic anaemia. Although folic acid may produce a haematopoietic response in patients with megaloblastic anaemia due to Vitamin B12, it fails to prevent the onset of subacute combined degeneration of the cord. Absorption by route of exposure: Oral: Folic acid is rapidly absorbed from the proximal part of the gastrointestinal tract following oral administration. It is mainly absorbed in the proximal portion of the small intestine. The naturally occurring folate polyglutamate is enzymatically hydrolyzed to monoglutamate forms in the gastrointestinal tract prior to absorption. The peak folate activity in blood after oral administration is within 30 to 60 minutes. Enterohepatic circulation of folate has been demonstrated. Distribution by route of exposure: Tetrahydrofolic acid and its derivatives are distributed in all body tissues. The liver contains half of the total body stores of folate and is the principal storage site. Metabolism: Folic acid once absorbed is acted upon by hepatic dihydrofolate reductase to convert to its metabolically active form which is tetrahydrofolic acid. Following absorption, folic acid is largely reduced and methylated in the liver to N-5 methyltetrahydrofolic acid, which is the main transporting and storage form of folate in the body. Larger doses may escape metabolism by the liver and appear in the blood mainly as folic acid. Elimination by route of exposure: Oral: Following oral administration of single doses of folic acid in health adults, only a trace amount of the drug appears in urine. Following administration of large doses, the renal tubular reabsorption maximum is exceeded and excess folate is excreted unchanged in urine. Small amounts of orally administered folic acid have been recovered from feces. Pharmacodynamics: Folic acid is transformed into different coenzymes that are responsible for various reactions of intracellular metabolism mainly conversion of homocysteine to methionine, conversion of serine to glycine, synthesis of thymidylate, histidine metabolism, synthesis of purines and utilization or generation of formate. In man, nucleoprotein synthesis and the maintenance of normal erythropoiesis requires exogenous folate. Folic acid is the precursor of tetrahydrofolic acid which is active and acts as a co-factor for 1-carbon transfer reactions in the biosynthesis of purines and thymidylates of nucleic acids. Adults: There is little data available on folic acid toxicity in humans. A case of two patients who showed exacerbation of psychotic behavior during treatment with folic acid has been reported. Cytomorphological effects of folic acid were studied using in-vitro establishment human oral epithelium. A concentration twice that used clinically did not induce marked cytotoxic reaction in cultured cells. The most pronounced changes were cultures which showed degenerating cells showing edema, increased translucency of the cytoplasm, flattened cells and atypical filaments. Interactions: Folic acid therapy may increase phenytoin metabolism in folate deficient patients resulting in decreased phenytoin serum concentration. It has also been reported that concurrent administration of folic acid and chloramphenicol in folate deficient patients may result in antagonism of the hematopoietic response to folic acid. The use of ethotoin or mephenytoin concurrently with folic acid may decrease the effects of hydantoins by increasing hydantoin metabolism. Trimethoprim acts as a folate antagonist by inhibiting dihydrofolate reductase, so in patients receiving this drug leucovorin calcium must be given instead of folic acid. Folic acid may also interfere with the effects of pyrimethamine. Aminopterin (4 aminofolic acid) and methotrexate (4 amino- 10 methylfolic acid) antagonizes reduction of folic acid to tetrahydrofolic acid. Methotrexate continues to be used as an antineoplastic drug whose activity may be dependent on blocking certain syntheses, of purines, in which folic acid is required, thereby depriving neoplastic cells of compounds essential for their proliferation. Calcium leucovorin is used therapeutically as a potent antidote for the toxic effects of folic acid antagonists used as antineoplastic agents. Methotrexate or pyrimethamine or triamterene also acts as folate antagonist by inhibiting dihydrofolic reductase. Analgesics, anticonvulsants, antimalarials and corticosteroids may cause folic acid deficiency. Main adverse effects: Allergic reactions to folic acid have been rarely reported including erythema, rash, itching, general malaise and bronchospasm. Adverse gastrointestinal and central nervous system effects have been reported in patients receiving 15 mg of folic acid daily for one month. ANIMAL/PLANT STUDIES: Mode of action: Folic acid is relatively non-toxic. Toxicity studies in mice showed that folic acid could cause convulsions, ataxia and weakness. Histopathological studies in some strains of mice showed that toxic doses may also cause acute renal tubular necrosis. A possible relationship between folic acid neurotoxicity and cholinergic receptors in the pyriform cortex and amygdala has been shown. Interactions The use of high dose folic acid concomitantly with pyrimethamine to prevent bone marrow depression may cause a pharmacodynamic antagonism of the antiparasitic effect of pyrimethamine. Nonsteroidal antiinflammatory drugs (NSAIDS), including ibuprofen, indomethacin, naproxen, mefenamic acid, piroxicam, and sulindac taken at high therapeutic dosages may exert antifolate activity. Folic acid supplementation in mice was found to augment the therapeutic activity and ameliorate the adverse reactions of the ... antifolate cancer chemotherapeutic agent lometrexol. The /daily/ use of folic acid ... was found to enhance the antidepressant action of fluoxetine ... For more Interactions (Complete) data for FOLIC ACID (17 total), please visit the HSDB record page. |
| References | |
| Additional Infomation |
Therapeutic Uses
Hematinics Folic acid is indicated for prevention and treatment of folic acid deficiency states , including megaloblastic anemia and anemias of nutritional origin, pregnancy, infancy, or childhood. Recommended intakes may be increased and /or supplementation may be necessary in the following persons or conditions (based on documented folic acid deficiency): Alcoholism, hemolytic anemia, chronic fever, gastrectomy, chronic hemodialysis, infants (low birth weight, breast-fed, or those receiving unfortified formulas such as evaporated milk or goats milk), Intestinal disease (celiac disease, tropical sprue, persistent diarrhea), malabsorption syndromes associated with hepatic-biliary disease (hepatic function impairment, alcoholism with cirrhosis), /and/ prolonged stress. MEDICATION (VET): ... To prevent macrocytic anemia, embryonic death, cervical paralysis, and perosis In chicks. For more Therapeutic Uses (Complete) data for FOLIC ACID (7 total), please visit the HSDB record page. Drug Warnings Allergic reactions to folic acid preparations have been reported rarely and have included erythema, rash, itching, general malaise, and bronchospastic respiratory difficulty. Adverse GI effects such as anorexia, nausea, abdominal distention, flatulence, and a bitter/bad taste and adverse CNS effects such as altered sleep patterns, difficulties concentrating, irritability, overactivity, excitement, mental depression, confusion, and impaired judgement have been reported rarely in patients receiving 15 mg of folic acid daily for one month. Decreased serum vitamin B12 concentration may occur in patients receiving prolonged folic acid therapy. Folic acid should be administered with extreme caution in patients with undiagnosed anemia, since folic acid may obscure the diagnosis of pernicious anemia by alleviating hematologic manifestations of the disease while allowing the neurologic complications to progress. This may result in severe nervous system damage before the correct diagnosis is made. For more Drug Warnings (Complete) data for FOLIC ACID (7 total), please visit the HSDB record page. Pharmacodynamics Folic acid is a water-soluble B-complex vitamin found in foods such as liver, kidney, yeast, and leafy, green vegetables. Also known as folate or Vitamin B9, folic acid is an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. In order to function properly within the body, folic acid must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted by anti-metabolite therapies such as [DB00563] as they function as DHFR inhibitors to prevent DNA synthesis in rapidly dividing cells, and therefore prevent the formation of DHF and THF. In general, folate serum levels below 5 ng/mL indicate folate deficiency, and levels below 2 ng/mL usually result in megaloblastic anemia. |
| Molecular Formula |
C19H19N7O6
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|---|---|
| Molecular Weight |
441.3975
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| Exact Mass |
441.14
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| Elemental Analysis |
C, 51.70; H, 4.34; N, 22.21; O, 21.75
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| CAS # |
59-30-3
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| Related CAS # |
70114-87-3 (Folic acid, methyl-); 134-05-4 (10-Formylfolic acid); 54931-98-5 (10-Thiofolic acid); 119770-54-6 (11-Deazahomofolic acid); 72254-43-4 (11-Oxahomofolic acid); 85597-18-8 ( 5,10-Dideazafolic acid); 111113-75-8 (5,6,7,8-Tetrahydro-8-deazahomofolic acid); 130327-67-2 ( 5-Deazaisofolic acid); 51989-25-4 ( 8-Deazafolic acid; NSC 173522); 111113-73-6 (8-Deazahomofolic acid); 14866-11-6 (Dihydrohomofolic acid); 83704-88-5 (HH-Folic acid is a derivative of vitamin B); 3566-25-4 (Homofolic acid); 11076-68-9 (Lyofolic acid); 29291-35-8 (Nitrosofolic acid; CCRIS 466); 88912-57-6 (Pyrrofolic acid); 135-16-0 (5,6,7,8-tetrahydrofolic acid; Tetrahydropteroylglutamic acid; th-folate; folate-H4); 5786-82-3 (Tetrahydrohomofolic acid); 52454-37-2 (10-Deazaaminopterin; 10-Deaza-aminopterin; NSC 311469; NSC-311469; NSC311469); 28459-40-7 (10-Formyldihydrofolate); 2800-34-2 (10-Formyltetrahydrofolic acid; 10-Formyl-THF; 10FTHF); 74163-10-3 ( 11-Thiohomoaminopterin, a close analog of 11-thiohomofolic acid); 85803-29-8 (2-Fluoroaminopterin); 5472-96-8 (3-Chloromethotrexate); 59904-24-4 (5-Methyldihydrofolate); 50998-20-4 (5-Methyltetrahydrofolate triglutamate); 73951-54-9 (6R-Leucovorin); 77739-71-0 (Acanthifolicin); 25312-31-6 (Aminoanfol, an antifolic acid compound); 31690-11-6 (Arfolitixorin free, an antifolate modulator); 149930-93-8 (Arfolitixorin sulfate); 154705-24-5 (Arfolitixorin sodium); 501332-69-0 (BGC-945); 115940-48-2 (Calcium dextrofolinate, calcium salt of a derivative of Folic Acid);26560-38-3 (Calcium methyltetrahydrofolate); 5854-11-5 (CB 3705; CB-3705; CB3705; 5,8-Dideazafolic acid); 76849-19-9 (CB 3717; CB-3717; CB3717; N(sup 10)-Propargyl-5,8-dideazafolic acid); 18921-73-8 (chlorasquin, an inhibitor of dihydrofolate reductase); 4033-27-6 (Dihydrofolate); 36093-88-6 (Dihydroaminopterin); 528-74-5 (Dichloromethotrexate); 6807-82-5 ( Diopterin, a folic acid analog); 1148151-21-6 [Folitixorin calcium, (6R)-]; 6484-89-5 (Folate sodium; Folvite sodium); 815587-59-8 [olitixorin calcium, (6S)-]; 133978-76-4 (Folitixorin sodium); 35409-55-3 (Hexaglutamate folate); 112887-62-4 (ICI 198583, an antifolate thymidylate synthase inhibitor); 31690-09-2 (Levomefolinic acid); 1423663-76-6 ( Levomefolate sodium); 1429498-11-2 ( Levomefolate magnesium); 58-05-9 ( Levoleucovorin free acid); 1492-18-8 ( Levoleucovorin calcium); 6035-45-6 ( Levoleucovorin calcium hydrate); 163254-40-8 ( Levoleucovorin sodium); 1141892-29-6 (Levoleucovorin sodium); 120408-07-3 (Lometrexol sodium); 106400-81-1 (Lometrexol free acid); 106400-18-4 (LY249543, the S-isomer of lometrexol); 136208-85-0 (LY249543, the S-isomer of lometrexol); 82339-36-4 (Lysine-iodoacetylmethotrexate, a Folic Acid Antagonist); 7413-34-5 ( Methotrexate disodium); 7532-09-4 (Methotrexate monosodium); 59-05-2 (Methotrexate free acid); 6745-93-3 (Methotrexate hydrate); 15475-56-6 (Methotrexate sodium); 66147-29-3 (Methotrexate 1-methyl ester); 67022-39-3 (Methotrexate 5-methyl este); 79573-48-1 (Mefox; (6RS)-Mefox); 2179-16-0 (Ninopterin); 41600-13-9 (NSC269401, the isotope labelled analog of Methotrexate Diglutamate; 41600-14-0 ( NSC341076 is the isotope labelled analog of Methotrexate Triglutamate); 2197232-28-1 (OSI-7904L,1843U89; racemic) 139987-54-5 (OSI-7904L,1843U89; free acid); 89-38-3 (Pteropterin); 6164-84-7 (Pteropterin monohydrate); 33611-85-7 ( Pteroylpentaglutamic acid); 112887-68-0 (Raltitrexed); 4299-28-9 (Tetrahydromethotrexate); 29701-38-0 (Triglutamate folate); 52128-35-5 (Trimetrexate)
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| PubChem CID |
135398658
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| Appearance |
Light yellow to yellow solid powder
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| Melting Point |
482 °F (decomposes) (NTP, 1992)
250 °C |
| LogP |
-1.1
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| Hydrogen Bond Donor Count |
6
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
9
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| Heavy Atom Count |
32
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| Complexity |
767
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C1=CC(=CC=C1C(=O)N[C@@H](CCC(=O)O)C(=O)O)NCC2=CN=C3C(=N2)C(=O)NC(=N3)N
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| InChi Key |
OVBPIULPVIDEAO-LBPRGKRZSA-N
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| InChi Code |
InChI=1S/C19H19N7O6/c20-19-25-15-14(17(30)26-19)23-11(8-22-15)7-21-10-3-1-9(2-4-10)16(29)24-12(18(31)32)5-6-13(27)28/h1-4,8,12,21H,5-7H2,(H,24,29)(H,27,28)(H,31,32)(H3,20,22,25,26,30)/t12-/m0/s1
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| Chemical Name |
(2S)-2-[[4-[(2-amino-4-oxo-3H-pteridin-6-yl)methylamino]benzoyl]amino]pentanedioic acid
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| Synonyms |
FA; N-(4-{[(2-amino-4-oxo-1,4-dihydropteridin-6-yl)methyl]amino}benzoyl)-L-glutamic acid; pteroyl-L-glutamic acid; folacin; pteroyl-L-glutamate; Folic acid; Vitamin B11; Vitamin B9; Vitamin Bc; Vitamin Be; Vitamin M
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
1M NaOH: ~100 mg/mL (~226.6 mM)
DMSO: ~33.3 mg/mL (~75.5 mM) H2O: < 0.1 mg/mL |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.71 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 20.8 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: 2.08 mg/mL (4.71 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.2655 mL | 11.3276 mL | 22.6552 mL | |
| 5 mM | 0.4531 mL | 2.2655 mL | 4.5310 mL | |
| 10 mM | 0.2266 mL | 1.1328 mL | 2.2655 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.
PREconception Folic Acid Clinical Efficacy (PREFACE) Trial
CTID: NCT06641245
Phase: N/A Status: Not yet recruiting
Date: 2024-10-21
Products are for research use only; We do not sell to patients
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