 Chemical Structure.png)
Physicochemical Properties
| Molecular Formula | 13C11H1215N2O2 |
| Molecular Weight | 217.131 |
| Exact Mass | 204.089 |
| CAS # | 202406-50-6 |
| Related CAS # | L-Tryptophan;73-22-3 |
| PubChem CID | 6305 |
| Appearance | White to off-white solid powder |
| Melting Point | 554 to 558 °F (Decomposes) (NTP, 1992) |
| LogP | -1.1 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 3 |
| Heavy Atom Count | 15 |
| Complexity | 245 |
| Defined Atom Stereocenter Count | 1 |
| SMILES | C(O)(=O)[C@H](CC1C2C(=CC=CC=2)NC=1)N |
| InChi Key | QIVBCDIJIAJPQS-VIFPVBQESA-N |
| InChi Code | InChI=1S/C11H12N2O2/c12-9(11(14)15)5-7-6-13-10-4-2-1-3-8(7)10/h1-4,6,9,13H,5,12H2,(H,14,15)/t9-/m0/s1 |
| Chemical Name | (2S)-2-amino-3-(1H-indol-3-yl)propanoic acid |
| 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) |
Biological Activity
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion (L)-Tryptophan with plant oils in soft gelatin capsules permitted lower dosage than with usual dosage form. Max of free tryptophan in serum was achieved in 1st hr whereas 4-5 times as much would be required with tablets or hard gelatin capsules. Absorption and Fate. Tryptophan is readily absorbed from the gastro-intestinal tract. Tryptophan is extensively bound to serum albumin. It is metabolized to serotonin and other metabolites, incl kynurenine derivatives, and excreted in the urine. Pyridoxine and ascorbic acid appear to be concerned in its metabolism. Although the free amino acids dissolved in the body fluids are only a very small proportion of the body's total mass of amino acids, they are very important for the nutritional and metabolic control of the body's proteins. ... Although the plasma compartment is most easily sampled, the concentration of most amino acids is higher in tissue intracellular pools. Typically, large neutral amino acids, such as leucine and phenylalanine, are essentially in equilibrium with the plasma. Others, notably glutamine, glutamic acid, and glycine, are 10- to 50-fold more concentrated in the intracellular pool. Dietary variations or pathological conditions can result in substantial changes in the concentrations of the individual free amino acids in both the plasma and tissue pools. /Amino acids/ After ingestion, proteins are denatured by the acid in the stomach, where they are also cleaved into smaller peptides by the enzyme pepsin, which is activated by the increase in stomach acidity that occurs on feeding. The proteins and peptides then pass into the small intestine, where the peptide bonds are hydrolyzed by a variety of enzymes. These bond-specific enzymes originate in the pancreas and include trypsin, chymotrypsins, elastase, and carboxypeptidases. The resultant mixture of free amino acids and small peptides is then transported into the mucosal cells by a number of carrier systems for specific amino acids and for di- and tri-peptides, each specific for a limited range of peptide substrates. After intracellular hydrolysis of the absorbed peptides, the free amino acids are then secreted into the portal blood by other specific carrier systems in the mucosal cell or are further metabolized within the cell itself. Absorbed amino acids pass into the liver, where a portion of the amino acids are taken up and used; the remainder pass through into the systemic circulation and are utilized by the peripheral tissues. /Amino acids/ For more Absorption, Distribution and Excretion (Complete) data for (L)-Tryptophan (9 total), please visit the HSDB record page. Metabolism / Metabolites Hepatic. In Hartnup disease ... tryptophane appear/s/ in urine due to defective renal and intestinal absorption of tryptophane ... It is an intermediary metabolite in the synthesis of serotonin (5-hydroxytryptamine) and 5-hydroxyindole acetic acid (HIAA). Patients with bladder cancer excreted significantly more kynurenic acid, acetylkynurenine, kynurenine, and 3-hydroxykynurenine after ingesting a loading dose of L-tryptophan than did control subjects with no known disease. Tryptophan is metabolized in the liver by tryptophan pyrrolase and tryptophan hydroxylase. Metabolites include hydroxytryptophan, which is then converted to serotonin, and kynurenine derivatives. Some tryptophan is converted to nicotinic acid and nicotinamide. Pyridoxine and ascorbic acid are cofactors in the decarboxylation and hydroxylation, respectively, of tryptophan; pyridoxine apparently prevents the accumulation of the kynurenine metabolites. Yields indole-3-pyruvic acid in man ... and in rats; yields tryptamine in guinea pigs. /From table/ For more Metabolism/Metabolites (Complete) data for (L)-Tryptophan (21 total), please visit the HSDB record page. Hepatic. Biological Half-Life The biological half-life of tryptophan was reported to be 15.8 hr. |
| Toxicity/Toxicokinetics |
Toxicity Summary A number of important side reactions occur during the catabolism of tryptophan on the pathway to acetoacetate. The first enzyme of the catabolic pathway is an iron porphyrin oxygenase that opens the indole ring. The latter enzyme is highly inducible, its concentration rising almost 10-fold on a diet high in tryptophan. Kynurenine is the first key branch point intermediate in the pathway. Kynurenine undergoes deamniation in a standard transamination reaction yielding kynurenic acid. Kynurenic acid and metabolites have been shown to act as antiexcitotoxics and anticonvulsives. A second side branch reaction produces anthranilic acid plus alanine. Another equivalent of alanine is produced further along the main catabolic pathway, and it is the production of these alanine residues that allows tryptophan to be classified among the glucogenic and ketogenic amino acids. The second important branch point converts kynurenine into 2-amino-3-carboxymuconic semialdehyde, which has two fates. The main flow of carbon elements from this intermediate is to glutarate. An important side reaction in liver is a transamination and several rearrangements to produce limited amounts of nicotinic acid, which leads to production of a small amount of NAD+ and NADP+. Interactions Acetylsalicylic acid reduced serum-protein binding of tryptophan in man, causing rise in free serum tryptophan. Changes in metabolic pattern also occurred, with increased urinary excretion of xanthurenic acid and 3-hydroxylkynurenine and decreased excretion of 3-hydroxyanthranilic acid. Although tryptophan has been given to patients receiving MAOIs in the belief that clinical efficacy may be improved, it should be noted that the adverse effects may also be potentiated. Use of tryptophan with drugs that inhibit the reuptake of serotonin may exacerbate the adverse effects of the latter and precipitate the serotonin syndrome. There have been occasional reports of sexual disinhibition in patients taking tryptophan with phenothiazines or benzodiazepines. For more Interactions (Complete) data for (L)-Tryptophan (16 total), please visit the HSDB record page. Non-Human Toxicity Values LD50 Rat ip 1634 mg/kg LD50 Mouse ip 4800 mg/kg |
| References |
[1]. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. |
| Additional Infomation |
Therapeutic Uses Tryptophan is a precursor of serotonin. Because CNS depletion of serotonin is considered to be involved in depression, tryptophan has been used in its treatment. Although it has been given alone, evidence of effectiveness is scant and tryptophan has generally been used as adjunctive therapy in depression. It has sometimes been given with pyridoxine and ascorbic acid, which are involved in its metabolism to serotonin /EXPTL USE/: Inhibition of Walker 256 intramuscular carcinoma in rats by admin of l-tryptophan. (L)-Tryptophan decreases sleep latency and slightly increases sleeping time without altering qualitative characteristics of polygraphic patterns during sleep in normal subjects. In insomniac patients, it increases sleeping time and decreases both sleep latency and number of awakenings. Beneficial effects were observed when L-tryptophan was administered to 2 patients with myoclonus. In each case suspension of methylcellulose and water containing 1 g of (L)-tryptophan/15 mL was prepared and administered orally at a level of 10 g daily in 5 divided doses. For more Therapeutic Uses (Complete) data for (L)-Tryptophan (11 total), please visit the HSDB record page. Drug Warnings Since serotonin plays a role in inducing and maintaining sleep, l-tryptophan has been administered orally to increase brain levels of serotonin. Although a dose of 1 g significantly decreased sleep latency and total time awake without altering sleep patterns, the hypnotic action is observed only during the early part of the sleep cycle, is unpredictable, and is not characterized by a satisfactory dose-response relationship. Because the hypnotic action has not been confirmed in other studies, this use of l-tryptophan must be considered investigational and the drug is not recommended in routine clinical practice. In order to avoid central serotonergic toxicity, tryptophan should not be used in patients also receiving a monoamine oxidase inhibitor or the serotonin uptake inhibitor, fluoxetine (Prozac). Tryptophan-containing products have been associated with the eosinophilia-myalgia syndrome. Other adverse effects that have been reported include nausea, headache, lightheadedness, and drowsiness. An increased incidence of bladder tumours has been reported in mice given l-tryptophan orally as well as in cholesterol pellets embedded in the bladder lumen. However, there was no increase in tumour incidence when only high-dose, oral tryptophan was given. Tryptophan has been associated with eosinophilia-myalgia syndrome; caution is advised in patients receiving the drug who develop some, but not all, of the symptoms of this syndrome. It should not be used in those with a history of eosinophilia-myalgia syndrome associated with tryptophan treatment. For more Drug Warnings (Complete) data for (L)-Tryptophan (7 total), please visit the HSDB record page. Pharmacodynamics Tryptophan is critical for the production of the body's proteins, enzymes and muscle tissue. It is also essential for the production of niacin, the synthesis of the neurotransmitter serotonin and melatonin. Tryptophan supplements can be used as natural relaxants to help relieve insomnia. Tryptophan can also reduce anxiety and depression and has been shown to reduce the intensity of migraine headaches. Other promising indications include the relief of chronic pain, reduction of impulsivity or mania and the treatment of obsessive or compulsive disorders. Tryptophan also appears to help the immune system and can reduce the risk of cardiac spasms. Tryptophan deficiencies may lead to coronary artery spasms. Tryptophan is used as an essential nutrient in infant formulas and intravenous feeding. Tryptophan is marketed as a prescription drug (Tryptan) for those who do not seem to respond well to conventional antidepressants. It may also be used to treat those afflicted with seasonal affective disorder (a winter-onset depression). Tryptopan serves as the precursor for the synthesis of serotonin (5-hydroxytryptamine, 5-HT) and melatonin (N-acetyl-5-methoxytryptamine). |
Solubility Data
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples. Injection Formulations (e.g. IP/IV/IM/SC) Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] *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. Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline) Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline) Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline) Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil) Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Oral Formulations Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). Oral Formulation 3: Dissolved in PEG400 Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose Oral Formulation 6: Mixing with food powders Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.6055 mL | 23.0277 mL | 46.0554 mL | |
| 5 mM | 0.9211 mL | 4.6055 mL | 9.2111 mL | |
| 10 mM | 0.4606 mL | 2.3028 mL | 4.6055 mL |