2860 T3D2818 Nortriptyline Nortriptyline hydrochloride, the <i>N</i>-demethylated active metabolite of amitriptyline, is a dibenzocycloheptene-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, nortriptyline does not affect mood or arousal, but may cause sedation. In depressed individuals, nortriptyline exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Secondary amine TCAs, such as nortriptyline, are more potent inhibitors of norepinephrine reuptake than tertiary amine TCAs, such as amitriptyline. TCAs also down-regulate cerebral cortical &beta;-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine-H<sub>1</sub> receptors, &alpha;<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Nortriptyline exerts less anticholinergic and sedative side effects compared to the tertiary amine TCAs, amitriptyline and clomipramine. Nortriptyline may be used to treat depression, chronic pain (unlabeled use), irritable bowel syndrome (unlabeled use), diabetic neuropathy (unlabeled use), post-traumatic stress disorder (unlabeled use), and for migraine prophylaxis (unlabeled use). 72-69-5 4543 C19H21N 263.167400 White powder. 213-215°C 8.74e-04 g/L Oral, well absorbed from the GI tract. Peak plasma concentrations occur 7-8.5 hours following oral administration. It is believed that nortriptyline either inhibits the reuptake of the neurotransmitter serotonin at the neuronal membrane or acts at beta-adrenergic receptors. Tricyclic antidepressants do not inhibit monoamine oxidase nor do they affect dopamine reuptake. Undergoes hepatic metabolism via the same pathway as other TCAs. Route of Elimination: Approximately one-third of a single orally administered dose is excreted in urine within 24 hours. Small amounts are excreted in feces via biliary elimination. Half Life: 16 to 90+ hours LD<sub>50</sub>=mg/kg (orally in rat) No indication of carcinogenicity to humans (not listed by IARC). For the treatment of depression, chronic pain, irritable bowel syndrome, sleep disorders, diabetic neuropathy, agitation and insomnia, and migraine prophylaxis. Symptoms of overdose include cardiac dysrhythmias, severe hypotension, shock, congestive heart failure, pulmonary edema, convulsions, and CNS depression, including coma. Changes in the electrocardiogram, particularly in QRS axis or width, are clinically significant indicators of tricyclic antidepressant toxicity. 2009-07-21T20:27:06Z 2026-03-31T19:06:55Z Nortriptyline C07274 7640 Nortriptyline DB00540 true CNCCC=C1C2=CC=CC=C2CCC2=CC=CC=C12 C19H21N InChI=1S/C19H21N/c1-20-14-6-11-19-17-9-4-2-7-15(17)12-13-16-8-3-5-10-18(16)19/h2-5,7-11,20H,6,12-14H2,1H3 PHVGLTMQBUFIQQ-UHFFFAOYSA-N 263.3767 263.167399677 Exogenous Solid 4.51 HMDB14680 CHEMBL445 4384 <p>Abraham Nudelman, &#8220;<span class="caps">ACID</span> <span class="caps">ADDITION</span> <span class="caps">SALT</span> OF A <span class="caps">NORTRIPTYLINE</span>-<span class="caps">GABA</span> <span class="caps">CONJUGATE</span> <span class="caps">AND</span> A <span class="caps">PROCESS</span> OF <span class="caps">PREPARING</span> <span class="caps">SAME</span>.&#8221; U.S. Patent US20130184347, issued July 18, 2013.</p> CHEM002216 DTXSID9023384 NS00010393 methyl(3-{tricyclo[9.4.0.0³,⁸]pentadeca-1(15),3,5,7,11,13-hexaen-2-ylidene}propyl)amine