Lisdexamfetamine
Identification
- Name
- Lisdexamfetamine
- Accession Number
- DB01255
- Type
- Small Molecule
- Groups
- Approved, Investigational
- Description
Also known as Vyvanse, lisdexamfetamine (L-lysine-d-amphetamine) is a prodrug of the psychostimulant d-amphetamine [4]. It is paired with the essential amino acid L-lysine. Lisdexamfetamine dimesylate increases attention span and decreases restlessness in children and adults who are overactive/hyperactive, cannot concentrate for long periods, or are easily distracted or impulsive [2].
As a central nervous system stimulant, lisdexamfetamine is utilized as an adjunct therapy in the treatment of attention deficit hyperactivity disorder (ADHD). As a prodrug, lisdexamfetamine was specifically engineered as an abuse-resistant product [10]. The mechanism by which this occurs is through delayed release after ingestion (unlike some other psychostimulant drugs, which may be abused). After oral administration and absorption, enzyme hydrolysis after contact with red blood cells metabolize lisdexamfetamine into L- lysine, a naturally occurring essential amino acid and active d-amphetamine, which is responsible for the drug’s pharmacological effects. Gastrointestinal pH does not affect this conversion, and the addition of the L-lysine slows the amount of d-amphetamine available in the circulation and central nervous system [10].
- Structure
Structure for Lisdexamfetamine (DB01255)
- Synonyms
- Lisdexamfetamine
- Product Ingredients
Ingredient UNII CAS InChI Key Lisdexamfetamine dimesylate SJT761GEGS 608137-33-3 CETWSOHVEGTIBR-FORAGAHYSA-N - Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Vyvanse Capsule 40 mg/1 Oral Physicians Total Care, Inc. 2009-03-20 Not applicable US 
Vyvanse Capsule 10 mg/1 Oral Shire LLC 2014-08-30 Not applicable US Vyvanse Capsule 70 mg/1 Oral Shire LLC 2007-02-23 Not applicable US Vyvanse Tablet, chewable 60 mg/1 Oral Shire LLC 2017-01-28 Not applicable US Vyvanse Capsule 10 mg Oral Shire Pharma Canada Ulc 2015-06-26 Not applicable Canada 
Vyvanse Capsule 10 mg/1 Oral Avera McKennan Hospital 2015-03-26 2018-06-07 US Vyvanse Capsule 50 mg/1 Oral Shire LLC 2007-02-23 Not applicable US Vyvanse Tablet, chewable 40 mg/1 Oral Shire LLC 2017-01-28 Not applicable US Vyvanse Capsule 40 mg Oral Shire Pharma Canada Ulc 2010-04-14 Not applicable Canada Vyvanse Capsule 70 mg/1 Oral Physicians Total Care, Inc. 2010-03-04 Not applicable US - Categories
- Agents producing tachycardia
- Agents that produce hypertension
- Amines
- Amphetamines
- Central Nervous System Agents
- Central Nervous System Stimulants
- Central Nervous System Stimulation
- Centrally Acting Sympathomimetics
- Cytochrome P-450 CYP2D6 Inhibitors
- Cytochrome P-450 CYP2D6 Inhibitors (weak)
- Cytochrome P-450 CYP2D6 Substrates
- Cytochrome P-450 Enzyme Inhibitors
- Dopamine Agents
- Dopamine Uptake Inhibitors
- Ethylamines
- Membrane Transport Modulators
- Nervous System
- Neurotransmitter Agents
- Neurotransmitter Uptake Inhibitors
- Phenethylamines
- Psychoanaleptics
- Psychostimulants, Agents Used for Adhd and Nootropics
- Serotonergic Drugs Shown to Increase Risk of Serotonin Syndrome
- Sympathomimetics
- UNII
- H645GUL8KJ
- CAS number
- 608137-32-2
- Weight
- Average: 263.3785
Monoisotopic: 263.199762437 - Chemical Formula
- C15H25N3O
- InChI Key
- VOBHXZCDAVEXEY-JSGCOSHPSA-N
- InChI
- InChI=1S/C15H25N3O/c1-12(11-13-7-3-2-4-8-13)18-15(19)14(17)9-5-6-10-16/h2-4,7-8,12,14H,5-6,9-11,16-17H2,1H3,(H,18,19)/t12-,14-/m0/s1
- IUPAC Name
- (2S)-2,6-diamino-N-[(2S)-1-phenylpropan-2-yl]hexanamide
- SMILES
- C[C@@H](CC1=CC=CC=C1)NC(=O)[C@@H](N)CCCCN
Pharmacology
- Indication
For the treatment of Attention-deficit/hyperactivity disorder (ADHD) and for moderate to severe binge eating disorder in adults [Label], [4].
This drug is not indicated for weight loss. Use of other sympathomimetic drugs for weight loss is associated with serious cardiovascular effects. The safety and effectiveness of this drug for the treatment of obesity have not yet been determined [Label].
- Associated Conditions
- Pharmacodynamics
Lisdexamfetamine dimesylate is a prodrug of d-amphetamine. Amphetamines are non-catecholamine sympathomimetic amines with CNS stimulating properties [Label]. This agent works primarily by inducing the release of the neurotransmitters dopamine and norepinephrine from their storage areas in presynaptic nerve terminals [9]. Both of these transmitters contribute to alertness, increased concentration, in addition to effort and motivation.
- Mechanism of action
Lisdexamfetamine is a prodrug of dextroamphetamine. The active form of this drug blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites for the reuptake of norepinephrine and dopamine in vitro [Label]. The mechanism of therapeutic action in attention deficit hyperactivity disorder (ADHD) is not fully understood [8], [Label]. Amphetamines have been recently found to target the trace amine-associated receptor 1 (TAAR1), which was recently discovered. This may explain some of its effects on the extraneuronal space [5], [6],[7]. Ultimately, the ability of this agent to increase synaptic concentrations of the catecholamine neurotransmitters noradrenaline and dopamine in the prefrontal cortex (PFC), and in the striatum, results in several behavioral changes [9], [Label].
Target Actions Organism UTrace amine-associated receptor 1 agonistHumans - Absorption
After oral administration, lisdexamfetamine is rapidly absorbed from the gastrointestinal tract [Label], [8].
Chewable tablet form: After a single dose of 60 mg a chewable tablet in healthy subjects under fasted conditions, the Tmax of lisdexamfetamine and dextroamphetamine was reached at about 1 hour and 4.4 hour post administration, respectively [Label].
Capsule form: Following single-dose oral (30 mg, 50 mg, or 70 mg) in patients ages 6 to 12 years with ADHD under fasted conditions, Tmax of lisdexamfetamine and dextroamphetamine was reached at about 1 hour and 3.5 hours post administration, respectively [Label].
- Volume of distribution
There is no accumulation of d-amphetamine (as measured by AUC) at steady state in healthy adults and no accumulation of lisdexamfetamine dimesylate after once-daily dosing for seven consecutive days [Label], [8].
- Protein binding
- Not Available
- Metabolism
THe conversion of Lisdexamfetamine dimesylate (LDX) to the active metabolite d-amphetamine occurs primarily in the blood through enzymatic cleavage after active absorption of LDX from the gastrointestinal lumen [4]. Lisdexamfetamine dimesylate is hydrolyzed in the blood to d-amphetamine, which is responsible for the drug’s therapeutic activity, as well as L-lysine. Amphetamine is reported to be oxidized at the 4 position of the benzene ring to form 4-hydroxyamphetamine, or on the side chain α or β carbons to form alpha-hydroxy-amphetamine or norephedrine, respectively. Norephedrine and 4-hydroxy-amphetamine are both active and each is subsequently oxidized to form 4-hydroxy-norephedrine. Alpha-hydroxy-amphetamine undergoes the process of deamination to form phenylacetone, which finally forms benzoic acid and its glucuronide and the glycine conjugate, hippuric acid. Although the enzymes involved in amphetamine metabolism have not been clearly identified, CYP2D6 is known to be involved with the formation of 4-hydroxy-amphetamine from amphetamine [8].
- Route of elimination
After the oral administration of a 70mg dose of radiolabeled lisdexamfetamine dimesylate to six healthy subjects, about 96% of the oral dose radioactivity was recovered in the urine and only 0.3% recovered in the feces [Label], [8].
- Half life
The mean plasma elimination half-life of dextroamphetamine was about 12 hours after oral administration of lisdexamfetamine dimesylate [Label].
The plasma elimination half-life of lisdexamfetamine alone averaged less than one hour in studies of lisdexamfetamine dimesylate administered in volunteer subjects [Label].
- Clearance
In a study of 47 subjects aged 55 years of age or older, amphetamine clearance was approximately 0.7L/hr/kg for subjects 55-74 years of age and 0.55L/hr/kg for subjects ≥75 years of age. This is slightly reduced compared to younger adults (approximately 1L/hr/kg for subjects 18-45 years of age) [8].
- Toxicity
Acute toxicity: Symptoms of acute overdosage with amphetamines include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia, and rhabdomyolysis. Fatigue and depression generally follow the symptoms central nervous system stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension and/or circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Lethal poisoning is usually preceded by convulsions and coma [Label]. Prescribers should consider that serious cardiovascular (CV) events have been reported with this class of drugs [8].
Long-term effects: Acute administration of high doses of amphetamine (d- or d,l-) has been shown to produce long-term neurotoxic effects, which include irreversible nerve fiber damage, in rodents. The relevance of these findings to humans is currently unknown [Label].
Oral LD50 (rat): 7,060 mg/kg [MSDS]
Oral LD50 (mouse): 3,450 mg/kg [MSDS]
Use in Pregnancy
This drug is categorized as a Pregnancy Category C: Animal studies have shown risk to the fetus, there are no controlled studies in women, or studies in women and animals are not available [Label].
- Affected organisms
- Humans and other mammals
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
Drug Interaction 1-(3-Mercapto-2-Methyl-Propionyl)-Pyrrolidine-2-Carboxylic Acid The risk or severity of hypertension can be increased when Lisdexamfetamine is combined with 1-(3-Mercapto-2-Methyl-Propionyl)-Pyrrolidine-2-Carboxylic Acid. 1-benzylimidazole The therapeutic efficacy of 1-benzylimidazole can be decreased when used in combination with Lisdexamfetamine. 2,5-Dimethoxy-4-ethylamphetamine The risk or severity of serotonin syndrome can be increased when Lisdexamfetamine is combined with 2,5-Dimethoxy-4-ethylamphetamine. 2,5-Dimethoxy-4-ethylthioamphetamine The risk or severity of serotonin syndrome can be increased when Lisdexamfetamine is combined with 2,5-Dimethoxy-4-ethylthioamphetamine. 3-isobutyl-1-methyl-7H-xanthine The risk or severity of adverse effects can be increased when Lisdexamfetamine is combined with 3-isobutyl-1-methyl-7H-xanthine. 3,4-Methylenedioxyamphetamine The risk or severity of serotonin syndrome can be increased when Lisdexamfetamine is combined with 3,4-Methylenedioxyamphetamine. 4-Bromo-2,5-dimethoxyamphetamine The risk or severity of serotonin syndrome can be increased when Lisdexamfetamine is combined with 4-Bromo-2,5-dimethoxyamphetamine. 4-Methoxyamphetamine The risk or severity of hypertension can be increased when Lisdexamfetamine is combined with 4-Methoxyamphetamine. 5-methoxy-N,N-dimethyltryptamine The risk or severity of serotonin syndrome can be increased when Lisdexamfetamine is combined with 5-methoxy-N,N-dimethyltryptamine. 6-O-benzylguanine The risk or severity of adverse effects can be increased when Lisdexamfetamine is combined with 6-O-benzylguanine. - Food Interactions
- Not Available
References
- Synthesis Reference
Michael J. Bauer, Gary Richard Callen, Judi Christine Humphrey, Todd Jeffrey Johnson, Matthew Wendell Schiesher, "Methods and Compositions for Preparing Lisdexamfetamine and Salts Thereof." U.S. Patent US20120157706, issued June 21, 2012.
US20120157706- General References
- Jasinski DR, Krishnan S: Human pharmacology of intravenous lisdexamfetamine dimesylate: abuse liability in adult stimulant abusers. J Psychopharmacol. 2009 Jun;23(4):410-8. doi: 10.1177/0269881108093841. Epub 2008 Jul 17. [PubMed:18635707]
- Madaan V: Lisdexamfetamine dimesylate for childhood ADHD. Drugs Today (Barc). 2008 May;44(5):319-24. doi: 10.1358/dot.2008.44.5.1215724. [PubMed:18548134]
- Krishnan S, Moncrief S: An evaluation of the cytochrome p450 inhibition potential of lisdexamfetamine in human liver microsomes. Drug Metab Dispos. 2007 Jan;35(1):180-4. Epub 2006 Oct 11. [PubMed:17035599]
- Goodman DW: Lisdexamfetamine dimesylate (vyvanse), a prodrug stimulant for attention-deficit/hyperactivity disorder. P T. 2010 May;35(5):273-87. [PubMed:20514273]
- Miller GM: The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. J Neurochem. 2011 Jan;116(2):164-76. doi: 10.1111/j.1471-4159.2010.07109.x. [PubMed:21073468]
- Liu JF, Li JX: TAAR1 in Addiction: Looking Beyond the Tip of the Iceberg. Front Pharmacol. 2018 Mar 27;9:279. doi: 10.3389/fphar.2018.00279. eCollection 2018. [PubMed:29636691]
- Pei Y, Asif-Malik A, Canales JJ: Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications. Front Neurosci. 2016 Apr 5;10:148. doi: 10.3389/fnins.2016.00148. eCollection 2016. [PubMed:27092049]
- Vyvanse, Canadian Monograph [File]
- EPAR: Lisdexamfetamine dimesylate [File]
- WHO Summary: Lisdexamfetamine [File]
- External Links
- Human Metabolome Database
- HMDB0015385
- PubChem Compound
- 11597698
- PubChem Substance
- 46505358
- ChEBI
- 135925
- ChEMBL
- CHEMBL1201222
- Therapeutic Targets Database
- DAP000571
- PharmGKB
- PA164748975
- RxList
- RxList Drug Page
- Drugs.com
- Drugs.com Drug Page
- Wikipedia
- Lisdexamfetamine
- ATC Codes
- N06BA12 — Lisdexamfetamine
- AHFS Codes
- 28:20.04 — Amphetamines
- FDA label
- Download (371 KB)
- MSDS
- Download (33.8 KB)
Clinical Trials
- Clinical Trials
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- New River Pharmaceuticals Inc.
- Patheon Inc.
- Physicians Total Care Inc.
- Quality Care
- Shire Inc.
- Dosage forms
Form Route Strength Capsule Oral 10 mg Capsule Oral 10 mg/1 Capsule Oral 20 mg Capsule Oral 20 mg/1 Capsule Oral 30 mg Capsule Oral 30 mg/1 Capsule Oral 40 mg/1 Capsule Oral 40 mg Capsule Oral 50 mg Capsule Oral 50 mg/1 Capsule Oral 60 mg/1 Capsule Oral 60 mg Capsule Oral 70 mg/1 Capsule Oral 70 mg Tablet, chewable Oral 10 mg/1 Tablet, chewable Oral 20 mg/1 Tablet, chewable Oral 30 mg/1 Tablet, chewable Oral 40 mg/1 Tablet, chewable Oral 50 mg/1 Tablet, chewable Oral 60 mg/1 - Prices
Unit description Cost Unit Vyvanse 30 mg capsule 6.24USD capsule Vyvanse 50 mg capsule 6.02USD capsule Vyvanse 70 mg capsule 5.85USD capsule Vyvanse 40 mg capsule 5.8USD capsule Vyvanse 20 mg capsule 5.26USD capsule Vyvanse 60 mg capsule 5.02USD capsule DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.- Patents
Patent Number Pediatric Extension Approved Expires (estimated) US7659253 No 2010-02-09 2023-02-24 US US7718619 No 2010-05-18 2023-02-24 US US7659254 No 2010-02-09 2023-02-24 US US7671030 No 2010-03-02 2023-02-24 US US7662788 No 2010-02-16 2023-02-24 US US7687467 No 2010-03-30 2023-02-24 US US7678770 No 2010-03-16 2023-02-24 US US7671031 No 2010-03-02 2023-02-24 US US7713936 No 2010-05-11 2023-02-24 US US7674774 No 2010-03-09 2023-02-24 US US7678771 No 2010-03-16 2023-02-24 US US7655630 No 2010-02-02 2023-02-24 US US7687466 No 2010-03-30 2023-02-24 US US7223735 No 2007-05-29 2023-02-24 US US7700561 No 2010-04-20 2023-02-24 US US7662787 No 2010-02-16 2023-02-24 US US7723305 No 2010-05-25 2023-02-24 US US7105486 No 2006-09-12 2023-02-24 US
Properties
- State
- Liquid
- Experimental Properties
Property Value Source water solubility 792 mg/mL (dimesylate salt) FDA label logP -1.76 https://www.tga.gov.au/sites/.../auspar-lisdexamfetamine-dimesilate-131023-pi.docx pKa 10.5 https://www.tga.gov.au/sites/.../auspar-lisdexamfetamine-dimesilate-131023-pi.docx - Predicted Properties
Property Value Source Water Solubility 0.0877 mg/mL ALOGPS logP 1.01 ALOGPS logP 1.14 ChemAxon logS -3.5 ALOGPS pKa (Strongest Acidic) 15.89 ChemAxon pKa (Strongest Basic) 10.21 ChemAxon Physiological Charge 2 ChemAxon Hydrogen Acceptor Count 3 ChemAxon Hydrogen Donor Count 3 ChemAxon Polar Surface Area 81.14 Å2 ChemAxon Rotatable Bond Count 8 ChemAxon Refractivity 78.31 m3·mol-1 ChemAxon Polarizability 31.28 Å3 ChemAxon Number of Rings 1 ChemAxon Bioavailability 1 ChemAxon Rule of Five Yes ChemAxon Ghose Filter Yes ChemAxon Veber's Rule No ChemAxon MDDR-like Rule No ChemAxon - Predicted ADMET features
Property Value Probability Human Intestinal Absorption + 0.9858 Blood Brain Barrier + 0.9444 Caco-2 permeable + 0.664 P-glycoprotein substrate Substrate 0.6919 P-glycoprotein inhibitor I Non-inhibitor 0.9264 P-glycoprotein inhibitor II Non-inhibitor 0.9802 Renal organic cation transporter Non-inhibitor 0.8398 CYP450 2C9 substrate Non-substrate 0.8303 CYP450 2D6 substrate Non-substrate 0.621 CYP450 3A4 substrate Non-substrate 0.7228 CYP450 1A2 substrate Non-inhibitor 0.7025 CYP450 2C9 inhibitor Non-inhibitor 0.9337 CYP450 2D6 inhibitor Non-inhibitor 0.858 CYP450 2C19 inhibitor Non-inhibitor 0.7568 CYP450 3A4 inhibitor Non-inhibitor 0.5499 CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.8494 Ames test Non AMES toxic 0.7156 Carcinogenicity Non-carcinogens 0.854 Biodegradation Not ready biodegradable 0.8575 Rat acute toxicity 2.0058 LD50, mol/kg Not applicable hERG inhibition (predictor I) Weak inhibitor 0.9688 hERG inhibition (predictor II) Non-inhibitor 0.9004
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
Spectrum Spectrum Type Splash Key Predicted GC-MS Spectrum - GC-MS Predicted GC-MS Not Available Predicted MS/MS Spectrum - 10V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 10V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Negative (Annotated) Predicted LC-MS/MS Not Available
Taxonomy
- Description
- This compound belongs to the class of organic compounds known as alpha amino acid amides. These are amide derivatives of alpha amino acids.
- Kingdom
- Organic compounds
- Super Class
- Organic acids and derivatives
- Class
- Carboxylic acids and derivatives
- Sub Class
- Amino acids, peptides, and analogues
- Direct Parent
- Alpha amino acid amides
- Alternative Parents
- Amphetamines and derivatives / Phenylpropanes / N-acyl amines / Secondary carboxylic acid amides / Organopnictogen compounds / Organic oxides / Monoalkylamines / Hydrocarbon derivatives / Carbonyl compounds
- Substituents
- Alpha-amino acid amide / Amphetamine or derivatives / Phenylpropane / Monocyclic benzene moiety / Fatty amide / Fatty acyl / Benzenoid / N-acyl-amine / Carboxamide group / Secondary carboxylic acid amide
- Molecular Framework
- Aromatic homomonocyclic compounds
- External Descriptors
- Not Available
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Agonist
- General Function
- Trace-amine receptor activity
- Specific Function
- Receptor for trace amines, including beta-phenylethylamine (b-PEA), p-tyramine (p-TYR), octopamine and tryptamine, with highest affinity for b-PEA and p-TYR. Unresponsive to classical biogenic amin...
- Gene Name
- TAAR1
- Uniprot ID
- Q96RJ0
- Uniprot Name
- Trace amine-associated receptor 1
- Molecular Weight
- 39091.34 Da
References
- Miller GM: The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. J Neurochem. 2011 Jan;116(2):164-76. doi: 10.1111/j.1471-4159.2010.07109.x. [PubMed:21073468]
- Liu JF, Li JX: TAAR1 in Addiction: Looking Beyond the Tip of the Iceberg. Front Pharmacol. 2018 Mar 27;9:279. doi: 10.3389/fphar.2018.00279. eCollection 2018. [PubMed:29636691]
- Pei Y, Asif-Malik A, Canales JJ: Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications. Front Neurosci. 2016 Apr 5;10:148. doi: 10.3389/fnins.2016.00148. eCollection 2016. [PubMed:27092049]
Enzymes
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- SubstrateInhibitor
- General Function
- Steroid hydroxylase activity
- Specific Function
- Responsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic...
- Gene Name
- CYP2D6
- Uniprot ID
- P10635
- Uniprot Name
- Cytochrome P450 2D6
- Molecular Weight
- 55768.94 Da
References
- Hutson PH, Pennick M, Secker R: Preclinical pharmacokinetics, pharmacology and toxicology of lisdexamfetamine: a novel d-amphetamine pro-drug. Neuropharmacology. 2014 Dec;87:41-50. doi: 10.1016/j.neuropharm.2014.02.014. Epub 2014 Mar 1. [PubMed:24594478]
- Tan-Kam T, Suthisisang C, Pavasuthipaisit C, Limsila P, Puangpetch A, Sukasem C: Importance of pharmacogenetics in the treatment of children with attention deficit hyperactive disorder: a case report. Pharmgenomics Pers Med. 2013;6:3-7. doi: 10.2147/PGPM.S36782. Epub 2013 Jan 11. [PubMed:23526481]
- Vyvanse FDA label [File]
Transporters
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Substrate
- Curator comments
- These data are based on in vitro studies.
- General Function
- Proton-dependent oligopeptide secondary active transmembrane transporter activity
- Specific Function
- Proton-coupled intake of oligopeptides of 2 to 4 amino acids with a preference for dipeptides. May constitute a major route for the absorption of protein digestion end-products.
- Gene Name
- SLC15A1
- Uniprot ID
- P46059
- Uniprot Name
- Solute carrier family 15 member 1
- Molecular Weight
- 78805.265 Da
References
- Pennick M: Absorption of lisdexamfetamine dimesylate and its enzymatic conversion to d-amphetamine. Neuropsychiatr Dis Treat. 2010 Jun 24;6:317-27. [PubMed:20628632]
- Elvanse EPAR [File]
Drug created on May 14, 2007 19:24 / Updated on February 13, 2019 05:18