Amitriptyline HCl

Catalog No.S3183

Amitriptyline HCl  Chemical Structure

Molecular Weight(MW): 313.86

Amitriptyline inhibits serotonin receptor, norepinephrine receptor, 5-HT4, 5-HT2 and sigma 1 receptor with IC50 of 3.45 nM, 13.3 nM, 7.31 nM, 235 nM and 287 nM, respectively.

Size Price Stock Quantity  
In DMSO USD 130 In stock
USD 97 In stock
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Biological Activity

Description Amitriptyline inhibits serotonin receptor, norepinephrine receptor, 5-HT4, 5-HT2 and sigma 1 receptor with IC50 of 3.45 nM, 13.3 nM, 7.31 nM, 235 nM and 287 nM, respectively.
Targets
Serotonin receptor [1] 5-HT4 [2] Norepinephrine receptor [1] 5-HT2 [3] Sigma 1 receptor [4]
3.45 nM 7.31 nM 13.3 nM 235 nM 287 nM
In vitro

Amitriptyline inhibits Forskolin-stimulated cyclic AMP accumulation with EC50 values of 16.2 μM in intact CHO/DOR cells. Amitriptyline causes a concentration-dependent stimulation of ERK1/2 and GSK-3β phosphorylation with EC50 values of 9.0 μM in CHO/DOR cells. Amitriptyline (15 μM) causes a stimulation of ERK1/2 phosphorylation in C6 cells. Amitriptyline (30 μM) inhibits Forskolin-stimulated adenylyl cyclase activity and antagonizes (−)-U50,488 inhibitory effect in rat nucleus accumbens. [5] Amitriptyline binds the extracellular domain of both TrkA and TrkB and promotes TrkA-TrkB receptor heterodimerization. Amitriptyline (< 500 nM) promotes TrkA autophosphorylation in primary neurons and induces neurite outgrowth in PC12 cells. Amitriptyline selectively protects T17 cells from apoptosis with EC50 of 50 nM. [6]

In vivo Amitriptyline (15 mg/kg, i.p.) activates TrkA and TrkB receptors and significantly reduces kainic acid-triggered neuronal cell death in mice. [6] Amitriptyline (15 mg/kg and 30 mg/kg, i.p.) dose-dependently decreases the immobility time in the forced swimming test (FST) of mice. Amitriptyline (15 mg/kg, i.p.) shows a significant 24-h rhythm in the immobility time in the forced swimming test (FST) of mice. [7] Amitriptyline (1 mg/kg and 3 mg/kg) significantly increases the total distance travelled of mice in novel cages. Amitriptyline (10 mg/kg p.o., twice daily) considerably attenuates the hypothermic response to 8-OHDPAT and mCPP in mice. Amitriptyline (10 mg/kg p.o., twice daily) significantly reduces serotonin transporter density by approximately 20% in cortex of mice. [8]

Protocol

Solubility (25°C)

In vitro DMSO 63 mg/mL (200.72 mM)
Ethanol 63 mg/mL (200.72 mM)
Water 15 mg/mL (47.79 mM)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 313.86
Formula

C20H23N.HCl

CAS No. 549-18-8
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02519400 Unknown status Drug: Amitriptyline Depression Asan Medical Center August 2015 Phase 1
NCT02101892 Completed Drug: Amitriptyline|Drug: placebo Migraine|Preventive Treatment Rambam Health Care Campus|Migraine Research Foundation April 2014 Not Applicable
NCT00516503 Completed Drug: baclofen/amitriptyline/ketamine gel|Other: placebo Chronic Myeloproliferative Disorders|Leukemia|Lymphoma|Lymphoproliferative Disorder|Multiple Myeloma and Plasma Cell Neoplasm|Myelodysplastic Syndromes|Myelodysplastic/Myeloproliferative Neoplasms|Neurotoxicity|Pain|Unspecified Adult Solid Tumor Protocol Specific Alliance for Clinical Trials in Oncology|National Cancer Institute (NCI) February 2008 Phase 3
NCT00471445 Completed Drug: ketamine/amitriptyline NP-H cream|Other: placebo Neurotoxicity|Pain|Peripheral Neuropathy|Unspecified Adult Solid Tumor Protocol Specific Gary Morrow|National Cancer Institute (NCI)|University of Rochester October 2007 Phase 3
NCT00991848 Completed Drug: Lidocaine Fibromyalgia|Chronic Pain Federal University of São Paulo January 2005 Phase 1

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5-HT Receptor Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID