Nutrabiotech Atomoxetine Hcl 98% 1G Powder, 98% high purity Atomoxetine Hcl powder, selective norepinephrine reuptake inhibitor, neural catecholamine regulator, attention and executive function research raw material

Nutrabiotech 99% powder Atomoxetine hydrochloride CAS 82248-59-7

High-purity Atomoxetine hydrochloride powder CAS 82248-59-7, a selective norepinephrine reuptake inhibitor compound. Widely used in neurological biochemical research, pharmaceutical intermediate synthesis, central nervous system mechanism study and laboratory scientific experiments. Features high solubility, stable chemical activity and reliable bulk raw material supply for global research institutions and pharmaceutical factories.
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Atomoxetine Hydrochloride (CAS 82248-59-7) Selective Norepinephrine Reuptake Inhibitor | sNRI, NET Inhibitor, Non-Stimulant ADHD Reference Standard

Atomoxetine HCl CAS 82248-59-7
Selective Norepinephrine Reuptake Inhibitor

A highly selective norepinephrine transporter (NET/SLC6A2) inhibitor and the first non-stimulant approved by the FDA for ADHD (2002). Atomoxetine produces a region-selective elevation of norepinephrine and dopamine in the prefrontal cortex without increasing dopamine in the nucleus accumbens or striatum — the pharmacological basis of its low abuse liability. A CYP2D6 substrate with a well-characterized poor-metabolizer phenotype, it is a cornerstone reference compound for noradrenergic, attention, and pharmacogenetics research.

Selective NRI (sNRI) NET / SLC6A2 Inhibitor Non-Stimulant Prefrontal DA Elevation CYP2D6 Substrate NMDA Receptor Blocker R(-) Enantiomer
Request a Quote Technical Specs
291.82
MW (C17H21NO·HCl)
≥98%
Purity (HPLC)
NET
Primary Target (SLC6A2)

Molecular Information

Name: Atomoxetine Hydrochloride
CAS (HCl): 82248-59-7
CAS (free base): 83015-26-3
Formula: C17H21NO·HCl
MW: 291.82 (salt) / 255.36 (base)
SMILES: CC1=C(C=CC=C1)O[C@H]
  (CCNC)C2=CC=CC=C2
InChIKey: LUCXVPAZUDVVBT
  -UNTBIKODSA-N
Chirality: R(-) isomer
Appearance: White to practically white solid
Synonyms: Atomoxetine HCl /
  Strattera (Eli Lilly)
Storage: Room temperature, dry
🧪
CAS Number
82248-59-7
⚖️
Molecular Weight
291.82
🎯
Primary Activity
Selective NRI
✅
Purity
≥98%

Product Technical Specifications

Complete physicochemical, pharmacokinetic and QC parameters for Atomoxetine Hydrochloride (CAS 82248-59-7)

📋 Physicochemical Properties

  • Product NameAtomoxetine Hydrochloride
  • IUPAC Name(-)-N-Methyl-3-phenyl-3-(o-tolyloxy)-propylamine hydrochloride
  • CAS (HCl salt)82248-59-7
  • CAS (free base)83015-26-3
  • SynonymsAtomoxetine HCl; Tomoxetine HCl; LY139603; Strattera
  • Molecular FormulaC17H21NO·HCl
  • Molecular Weight291.82 (salt) / 255.36 (base)
  • SMILES (free base)CC1=C(C=CC=C1)O[C@H](CCNC)C2=CC=CC=C2
  • InChIKey (HCl)LUCXVPAZUDVVBT-UNTBIKODSA-N
  • Optical RotationR(-) isomer, levorotatory
  • AppearanceWhite to practically white solid
  • SolubilityWater 27.8 mg/mL; DMSO; Ethanol
  • Drug ClassSelective norepinephrine reuptake inhibitor (sNRI)
  • HS Code2922.19

🔬 Quality Control, PK & Handling

  • Purity (HPLC)≥98%
  • FormCrystalline solid / powder
  • Oral Bioavailability63–94%
  • Elimination Half-life~5 h (CYP2D6 EM) / ~24 h (CYP2D6 PM)
  • Plasma Protein Binding98% (mainly albumin)
  • Primary MetabolismCYP2D6 → 4-hydroxyatomoxetine
  • Storage ConditionRoom temperature, dry, sealed
  • ShippingAmbient; desiccated packaging
  • QC DocumentationCOA / HPLC / NMR / MS / MSDS
  • Pack Sizes1g / 5g / 10g / 100g / 1KG
  • Stock StatusIn Stock
  • Use StatementResearch use only; not for human/clinical use

Key Molecular Targets & Transporter Selectivity Profile

Atomoxetine's defining feature is its high selectivity for the norepinephrine transporter over dopamine and serotonin transporters and over monoamine receptors

🧬 NET / SLC6A2 (Primary) 🔁 SERT / SLC6A4 (Weak) 🚫 DAT / SLC6A3 (Very Weak) 🧠 NMDA Receptor (Blocker) ⚡ Prefrontal Cortex DA 🧫 CYP2D6 (Substrate) 🔬 CYP2C19 (Minor Route) 📊 α2-Adrenoceptor (Indirect) 🛡️ Locus Coeruleus Signaling 🧽 Executive Function Circuits 💠 No Direct Monoamine Release 🔒 Low Reinforcement Liability

How Atomoxetine Works: Selective Noradrenergic Modulation of the Prefrontal Cortex

Atomoxetine's therapeutic profile emerges from three linked pharmacological principles — transporter selectivity, regional dopamine specificity, and sustained tonic modulation

1

Selective NET Blockade

Atomoxetine binds the presynaptic norepinephrine transporter (NET, SLC6A2) with high affinity, blocking reuptake of norepinephrine into the presynaptic terminal and raising synaptic NE. Affinity for SERT is substantially lower and for DAT lower still, giving a clean noradrenergic signature.

2

Region-Selective Dopamine Increase

In the prefrontal cortex, dopamine is cleared predominantly by NET rather than DAT because DAT expression is sparse. NET blockade therefore raises both NE and DA in the PFC — while leaving dopamine in the nucleus accumbens and striatum unchanged (Bymaster et al., 2002), which explains its low abuse liability.

3

Sustained Tonic Modulation

Rather than producing acute phasic monoamine surges like stimulants, atomoxetine delivers continuous tonic enhancement of catecholamine signaling. Clinical benefit accumulates over 2–4 weeks, consistent with adaptive changes in α2A/α1 receptor signaling and prefrontal network efficiency.

🧠 Secondary Pharmacology

  • SERT BindingMeasurable but lower affinity; may contribute to mood effects
  • NMDA ReceptorNon-competitive blockade reported at higher concentrations
  • Receptor PanelNo meaningful affinity for muscarinic, histaminic, or adrenergic receptors
  • Monoamine ReleaseNot a releasing agent (unlike amphetamine)
  • Reward CircuitNo accumbal DA elevation → non-controlled substance

🧫 CYP2D6 Pharmacogenetic Profile

  • Primary EnzymeCYP2D6
  • Main Metabolite4-Hydroxyatomoxetine (equipotent, low exposure)
  • Poor Metabolizers (PM)~7% of Caucasians; 1–2% East Asian
  • PM Exposure~10× higher AUC vs extensive metabolizers
  • Half-life EM vs PM~5 h vs ~24 h
  • Interaction RiskPotent CYP2D6 inhibitors (paroxetine, fluoxetine, quinidine)

Research Applications & Disease Models

Atomoxetine is used across neuropsychopharmacology, cognitive neuroscience, pediatric research and pharmacogenetics as a selective noradrenergic probe

🎯

ADHD — First-Line Non-Stimulant

The first non-stimulant approved by the FDA for ADHD (2002), indicated in children aged ≥6 years, adolescents and adults. Used as the benchmark comparator in non-stimulant efficacy studies, in patients with comorbid tics, anxiety, or substance use history, and where stimulant diversion is a concern.

FDA Approved 2002
🧬

Norepinephrine Transporter Biology

A gold-standard selective NET (SLC6A2) inhibitor for transporter binding assays, uptake inhibition studies, occupancy PET imaging, and knockout/knock-in mouse validation. Widely used to dissect noradrenergic contributions to arousal, attention and stress physiology.

NET / SLC6A2
🧠

Prefrontal Cortex Dopamine Research

Microdialysis studies (Bymaster et al., Neuropsychopharmacology 2002) established that atomoxetine elevates prefrontal DA and NE while leaving nucleus accumbens and striatal DA unchanged — a defining model for studying region-specific catecholamine regulation and abuse liability.

Region-Selective DA
🧫

CYP2D6 Pharmacogenetics

A canonical CYP2D6 probe substrate. Poor metabolizers show ~10-fold higher AUC and prolonged half-life, making atomoxetine a model compound for genotype-guided dosing, phenotype–genotype correlation studies, DDI modeling, and PBPK simulation work.

Pharmacogenomics
👶

Pediatric Psychopharmacology

Extensive pediatric evidence base including Kratochvil et al. (JAACAP 2002). Used in studies of growth, cardiovascular safety, long-term tolerability and dose-response in children and adolescents, and as a reference agent in pediatric clinical trial design.

Age ≥6 Years
🤝

Combination & Adjunct Therapy

Investigated as an adjunct to psychostimulants in partial responders, and in combination with α2A agonists (guanfacine, clonidine). Research explores complementary tonic (atomoxetine) versus phasic (stimulant) catecholamine modulation.

Adjunct Research
🌧️

Depression & Augmentation

Investigational use as a noradrenergic augmentation strategy in treatment-resistant depression and in ADHD with comorbid mood symptoms. Its SERT affinity and NE-mediated effects make it a useful probe of noradrenergic contributions to affective regulation.

Investigational
🔎

Cognitive Neuroscience

Widely used in human and animal studies of sustained attention, response inhibition, stop-signal reaction time, working memory and executive function. A key pharmacological tool for probing the noradrenergic locus coeruleus–prefrontal axis.

Executive Function
⚗️

Analytical & Reference Standard Use

Used as an analytical reference standard for HPLC/UPLC-MS method development, chiral purity determination of the R(-) enantiomer, impurity profiling, dissolution testing, and bioanalytical assay validation in plasma and urine matrices.

Reference Standard

Key Literature & Landmark Publications

Seminal papers on atomoxetine's mechanism, clinical efficacy, and pharmacogenetics

Michelson D, Adler L, Spencer T, et al. Atomoxetine in adults with ADHD: two randomized, placebo-controlled studies. American Journal of Psychiatry / Biological Psychiatry. 2003;53(2):112-120.
Adult ADHD pivotal program — efficacy and tolerability in adults
Kratochvil CJ, Heiligenstein JH, Dittmann R, et al. Atomoxetine and methylphenidate treatment in children with ADHD: a prospective, randomized, open-label trial. Journal of the American Academy of Child & Adolescent Psychiatry (JAACAP). 2002;41(7):776-784.
doi: 10.1097/00004583-200207000-00008
Bymaster FP, Katner JS, Nelson DL, et al. Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: a potential mechanism for efficacy in attention deficit/hyperactivity disorder. Neuropsychopharmacology. 2002;27(5):699-711.
doi: 10.1016/S0893-133X(02)00346-9
Michelson D, Faries D, Wernicke J, et al. Atomoxetine in the treatment of children and adolescents with ADHD: a randomized, placebo-controlled, dose-response study. Pediatrics. 2001;108(5):E83.
doi: 10.1542/peds.108.5.e83
Sauer JM, Ring BJ, Witcher JW. Clinical pharmacokinetics of atomoxetine. Clinical Pharmacokinetics. 2005;44(6):571-590.
doi: 10.2165/00003088-200544060-00002
Ring BJ, Gillespie JS, Eckstein JA, Wrighton SA. Identification of the human cytochromes P450 responsible for atomoxetine metabolism. Drug Metabolism and Disposition. 2002;30(3):319-323.
doi: 10.1124/dmd.30.3.319
Chamberlain SR, Müller U, Blackwell AD, et al. Neurochemical modulation of response inhibition and probabilistic learning in humans. Science. 2006;311(5762):861-863.
doi: 10.1126/science.1121218
Wong DT, Threlkeld PG, Best KL, Bymaster FP. A new inhibitor of norepinephrine uptake devoid of affinity for receptors in rat brain. Journal of Pharmacology and Experimental Therapeutics. 1982;222(1):61-65.
Original discovery paper describing tomoxetine/atomoxetine selectivity

Available Sizes & Ordering

Research-grade Atomoxetine Hydrochloride (CAS 82248-59-7) with full QC documentation; research packs and bulk custom quantities supported

TierPack SizeStock StatusSuitable ForLead Time
Standard1 gIn StockReceptor binding & uptake assaysSame/next-day ship
Medium5 gIn StockIn vivo behavioral pharmacology, microdialysisSame/next-day ship
Large10 gIn StockMulti-lab collaborations, chronic dosing studiesSame/next-day ship
Bulk100 gIn StockFormulation and process developmentQuote to confirm
Industrial1 KGMade to orderPilot/production scale, CMO supplyBatch delivery

💡 Reference sizes shown above; for exact pricing and availability please contact us for a quote. Bulk orders qualify for tiered discounts.

Frequently Asked Questions (FAQ)

What is Atomoxetine Hydrochloride (CAS 82248-59-7)?
Atomoxetine Hydrochloride is the HCl salt of atomoxetine, a highly selective norepinephrine reuptake inhibitor (sNRI) with molecular formula C17H21NO·HCl and molecular weight 291.82 (free base 255.36, CAS 83015-26-3). It is the R(-) enantiomer of tomoxetine and was the first non-stimulant approved by the FDA for ADHD in 2002, marketed as Strattera by Eli Lilly. Its IUPAC name is (-)-N-methyl-3-phenyl-3-(o-tolyloxy)-propylamine hydrochloride.
How does Atomoxetine differ from stimulants like methylphenidate or amphetamine?
Three key differences. Mechanism: atomoxetine blocks the norepinephrine transporter selectively; stimulants act primarily on the dopamine transporter and (for amphetamine) drive vesicular monoamine release. Regional selectivity: atomoxetine raises DA only in the prefrontal cortex, not in the nucleus accumbens or striatum, whereas stimulants elevate DA throughout reward circuitry. Time course: atomoxetine provides continuous tonic coverage with onset over 2–4 weeks, while stimulants act within hours. Consequently, atomoxetine is not a controlled substance and carries minimal abuse or diversion risk.
Why is CYP2D6 genotype so important for Atomoxetine?
Atomoxetine is metabolized principally by CYP2D6 to 4-hydroxyatomoxetine (with CYP2C19 as a minor pathway). Approximately 7% of Caucasians and 1–2% of East Asian populations are poor metabolizers (PM) carrying two non-functional alleles. PM individuals exhibit roughly 10-fold higher plasma AUC, higher peak concentrations, and an elimination half-life extended from about 5 hours (extensive metabolizers) to about 24 hours. Co-administration of strong CYP2D6 inhibitors such as paroxetine, fluoxetine, or quinidine phenocopies the PM state. This makes atomoxetine one of the most studied model substrates in CYP2D6 pharmacogenetics.
Does Atomoxetine have abuse potential?
No meaningful abuse potential has been demonstrated. The pharmacological basis is regional: in the prefrontal cortex dopamine is cleared largely by NET (DAT expression is sparse), so NET blockade raises prefrontal DA. In the nucleus accumbens and striatum, dopamine clearance is DAT-dependent, and atomoxetine leaves DA there unchanged (Bymaster et al., 2002). Because reinforcement depends on accumbal dopamine surges, atomoxetine produces no euphoria and is not scheduled as a controlled substance, making it valuable in patients with comorbid substance use disorder.
How quickly does Atomoxetine take effect?
Atomoxetine has a characteristically delayed onset. Although NET occupancy occurs rapidly after dosing, clinically meaningful symptom reduction typically emerges over 2 to 4 weeks of continuous daily administration, with maximal response frequently observed at 6 to 12 weeks. This lag is attributed to downstream adaptive changes in α2A/α1-adrenoceptor signaling and prefrontal network reorganization rather than acute transporter blockade alone. In research designs, chronic dosing paradigms are therefore preferred over single-dose challenges for efficacy endpoints.
Is Atomoxetine appropriate for pediatric research?
Yes. Atomoxetine is approved for ADHD in children aged 6 years and older, adolescents and adults, and has one of the largest pediatric datasets of any non-stimulant CNS agent. Key studies include the dose-response trial of Michelson et al. (Pediatrics 2001) and the comparative open-label trial of Kratochvil et al. (JAACAP 2002) versus methylphenidate. Pediatric research topics include growth trajectory, cardiovascular parameters, long-term tolerability, and weight-based dosing (typically titrated to a target mg/kg/day).
What are Atomoxetine's key pharmacokinetic parameters?
Oral bioavailability: 63–94% (lower in extensive metabolizers due to first-pass CYP2D6 metabolism, near-complete in poor metabolizers). Protein binding: 98%, predominantly to albumin. Half-life: ~5 hours in extensive metabolizers, ~24 hours in poor metabolizers. Metabolism: CYP2D6-mediated aromatic ring hydroxylation to 4-hydroxyatomoxetine, which is equipotent at NET but circulates at very low concentrations due to rapid glucuronidation. Food does not meaningfully affect overall exposure.
How should Atomoxetine HCl be dissolved and stored for laboratory use?
Atomoxetine hydrochloride is notably water soluble (~27.8 mg/mL), which distinguishes it from many CNS small molecules, and it also dissolves readily in DMSO and ethanol. For in vitro assays, aqueous buffer or a low-percentage DMSO stock diluted into media (final DMSO ≤0.1% v/v) both work well. For in vivo work, saline or water vehicles are commonly used. Store the solid at room temperature in a dry, sealed container; prepare aqueous solutions fresh or aliquot and freeze at −20°C to avoid repeated freeze–thaw cycles.
What is the significance of the R(-) enantiomer?
Atomoxetine is the R(-) (levorotatory) enantiomer of tomoxetine and is roughly an order of magnitude more potent at NET than the S(+) enantiomer. Because pharmacological activity is concentrated in one enantiomer, chiral purity is a critical quality attribute. Analytical workflows typically use chiral HPLC to confirm enantiomeric excess, and the racemate or S(+) isomer may be employed as a negative control in selectivity experiments.
Is QC documentation provided? Can I request a sample?
Every batch ships with a Certificate of Analysis (COA) including HPLC purity, NMR structural confirmation, and MS data. MSDS/SDS, chiral purity data, solubility datasheets, and Certificates of Origin are available on request. Sample evaluation is available for qualified institutions — please contact us for details.

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