Nortriptyline
(Synonyms: 去甲替林,Desmethylamitriptyline; Desitriptilina) 目录号 : GC64076
Nortriptyline hydrochloride (Desitriptyline, ELF-101, EN-7048, Desmethylamitriptyline) is the hydrochloride salt form of nortriptyline, a tricyclic antidepressant agent used for short-term treatment of various forms of depression.
Cas No.:72-69-5
Sample solution is provided at 25 µL, 10mM.
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Nortriptyline hydrochloride (Desitriptyline, ELF-101, EN-7048, Desmethylamitriptyline) is the hydrochloride salt form of nortriptyline, a tricyclic antidepressant agent used for short-term treatment of various forms of depression.
Nortriptyline inhibits the vascular Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake inhibition[1]. It is a tricyclic antidepressant. At the cellular level, nortriptyline is inhibitory to many proteins and responses such as astroglial inwardly rectifying Kir4.1 channels, human neutrophil phagocytosis and oxidative burst, human cytochrome P-450 enzymes, opioid receptors, Ca2+-activated K+ channels, and priming of human neutrophils. Nortriptyline induces a significant [Ca2+]i rise and decreases viability in PC3 cells, MG63 human osteosarcoma, and renal tubular cells[2]. Nortriptyline also exhibits anticancer activity in several different types of cells. For example,in human cutaneous melanoma cells,NTP has a half maximal inhibitory concentration(IC50) of 9 μM compared with 27 μM and 33 μM for clomipramine and amitriptyline, respectively. Nortriptyline induces cell cycle arrest and apoptosis in TCCSUP and MBT-2 cells[3].
Nortriptyline inhibits tumor growth in mice inoculated with MBT-2 cells. Low concentrations of NTP (0.1-5 μM) confer neuroprotective effects, downregulate cytosolic phospholipase A2, and prevent mitochondrial depolarization with minimal toxicity in both astrocytes and mice. In contrast, higher concentrations of NTP (10-50 μM) have anti-tumor effects on human osteosarcoma and cutaneous melanoma cells[3].
[1] Shin SE, et al. Korean J Physiol Pharmacol. 2017, 21(2):225-232. [2] Chih-Chuan Pan, et al. Drug Development Research. 2010, 71:323-330. [3] Yuan SY, et al. Eur J Pharmacol. 2015, 761:309-20.
| Cas No. | 72-69-5 | SDF | Download SDF |
| 别名 | 去甲替林,Desmethylamitriptyline; Desitriptilina | ||
| 分子式 | C19H21N | 分子量 | 263.38 |
| 溶解度 | 储存条件 | 4°C, protect from light | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.7968 mL | 18.984 mL | 37.968 mL |
| 5 mM | 0.7594 mL | 3.7968 mL | 7.5936 mL |
| 10 mM | 0.3797 mL | 1.8984 mL | 3.7968 mL |
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Should Nortriptyline be used as a first-line aid to help smokers quit? Results from a systematic review and meta-analysis
Addiction 2005 Mar;100(3):317-26.PMID:15733245DOI:10.1111/j.1360-0443.2005.00998.x.
Objectives: The objective of this paper is to evaluate the efficacy of Nortriptyline for smoking cessation compared to placebo and bupropion sustained release. Data sources: Randomized trials were identified by (1) checking electronic and (2) online publicly accessible registers of clinical trials; (3) searching references of identified studies and screening abstract books of conferences and symposia, and (4) personal communication with the first authors of identified papers. Review methods: We included randomized trials in which Nortriptyline was compared to placebo or bupropion hydrochloride SR. The main clinical outcome measure was (at least) 6-month prolonged abstinence, confirmed with a biochemical test. To investigate the efficacy of Nortriptyline in time, we calculated the percentage of smokers who relapsed in time. Results: We identified five randomized trials, including 861 smokers. Compared to placebo medication, Nortriptyline resulted in significantly higher prolonged abstinence rates after at least 6 months [relative risk (RR) = 2.4, 95% CI 1.7-3.6; RD = 0.11, 95% CI 0.07-0.15]. The difference in efficacy between Nortriptyline and placebo was highest in the first months after the target quit date. However, the number of people who remained abstinent decreased substantially and significantly faster over time in the Nortriptyline group. Although bupropion resulted in higher abstinence rates compared with Nortriptyline, the difference was not statistically significant (RR = 1.7, 95% CI 0.7-4.1). Conclusion: This systematic review and meta-analysis shows that the use of Nortriptyline for smoking cessation resulted in higher prolonged abstinence rates after at least 6 months compared to placebo treatment. Furthermore, the use of Nortriptyline for smoking cessation is well tolerated and safe. As a result, we believe health care professionals should be recommended to prescribe Nortriptyline as a first-line therapy for smoking cessation, also because of the much lower cost of Nortriptyline compared to bupropion SR.
Nortriptyline pharmacokinetics and plasma levels: implications for clinical practice
J Clin Psychiatry 1985 Oct;46(10):418-24.PMID:3900052doi
The pharmacokinetics of TCAs are reviewed with particular emphasis on Nortriptyline, the agent most extensively studied. The clinical uses of TCA plasma level-response studies are discussed in relationship to rational dosage adjustment to increase response rates and avoid iatrogenic toxicity. Other important topics discussed include the issue of active metabolites, single-dose prediction studies, and special considerations in treating the elderly and the medically ill.
Safety of Nortriptyline at equivalent therapeutic doses for smoking cessation: a systematic review and meta-analysis
Drug Saf 2011 Mar 1;34(3):199-210.PMID:21332244DOI:10.2165/11585950-000000000-00000.
Background: The limited use of Nortriptyline for smoking cessation is likely due to concerns about its serious adverse effects. Objective: To examine the safety of Nortriptyline at doses equivalent to those used in aiding smoking cessation. Data sources: A systematic search of relevant articles in MEDLINE, EMBASE, the Cochrane Database of Systematic Reviews, CINAHL, PsychINFO, WHO publications and the Clinical Trials database (through November 2008). Study selection: All studies of Nortriptyline at doses between 75 and 100 mg in any indication were reviewed. Data extraction: The quality of included studies was assessed based on the Jadad score. Data were extracted using a data extraction form. Data synthesis: From 442 potentially relevant articles identified, 17 studies met our selection criteria and were included for data analysis. Indications for Nortriptyline in these studies were smoking cessation (eight studies), depression (five studies), neuropathic pain (three studies) and schizophrenia (one study). 2885 individuals participated in these studies, with exposure time ranging between 4 and 12 weeks. The major comparator used in these trials was placebo. Overall, no life-threatening events occurred in these studies. Orthostatic hypotension was significantly higher in Nortriptyline users than in comparator groups (relative risk 2.8; 95% CI 1.4, 5.3). Other adverse events significantly associated with Nortriptyline were anticholinergic-related effects including drowsiness, dizziness, gastrointestinal disturbance and dysgeusia. Conclusions: Current evidence suggests that Nortriptyline, at doses between 75 and 100 mg, is not significantly associated with serious adverse events when administered in patients without underlying cardiovascular disease.
Nortriptyline enhances corticosteroid sensitivity of blood T cells from patients with chronic obstructive pulmonary disease
J Physiol Pharmacol 2021 Oct;72(5).PMID:35288481DOI:10.26402/jpp.2021.5.14.
Steroid unresponsiveness is a significant problem in the management of chronic obstructive pulmonary disease (COPD). The tricyclic antidepressant Nortriptyline has been reported to reverse corticosteroid resistance induced by oxidative stress. This study examined the potential synergistic anti-inflammatory effects of Nortriptyline and corticosteroids in T lymphocytes from patients with COPD and the molecular mechanisms underlying their action. Peripheral blood mononuclear cells (PBMCs) or whole blood cells from COPD patients were incubated with budesonide, Nortriptyline, or their combinations and stimulated with phytohaemagglutinin (PHA) or phorbol myristate acetate (PMA) plus ionomycin. The release of interleukin 4 (IL-4), IL-5, IL-8 and other mediators from PBMCs was measured by ELISA. Intracellular pro-inflammatory cytokines, glucocorticoid receptor (GR) and its isoform GRβ, histone deacetylase 2 (HDAC2), phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and p65 nuclear factor-κ (p65 NF-κB) were determined in CD4+ and CD8+ T cells using flow cytometry. Nortriptyline 10 μM decreased PHA-induced release of cytokines: IL-4, IL-5, IL-13, IL-17A, IL-33, macrophage migration inhibitory factor and thymic stromal lymphopoietin (TSLP). This drug alone also reduced the percentage of IL-4, IL-8, interferon gamma (IFNγ) positive CD4+ T cells and IL-4, IL-8 expressing CD8+ T cells stimulated with PMA/ionomycin, whereas Nortriptyline 1 μM had less pronounced effect. The combination of budesonide 10 nM with Nortriptyline 10 μM was more potent at suppressing IL-4, IL-5, IL-8, IL-13, IL-17A, TSLP secretion from PBMCs, as well as IL-4, IL-8, IFNγ, GRβ expression by CD4+ and CD8+ T cells when compared with single budesonide treatment. The association of budesonide 10 nM and Nt (1 μM to 10 μM) effectively decreased p38 MAPK and p65 NF-κB phosphorylation and increased HDAC2 expression in both CD4+ and CD8+ T cells. In conclusion, Nortriptyline alone demonstrates anti-inflammatory effects on blood T lymphocytes from COPD patients. Nortriptyline may also potentiate the effects of glucocorticoids and overcome corticosteroid insensitivity.
Influence of adjuvant Nortriptyline on the efficacy of electroconvulsive therapy: A randomized controlled trial and 1-year follow-up
Acta Psychiatr Scand 2022 May;145(5):517-528.PMID:35152416DOI:10.1111/acps.13408.
Objective: There is limited evidence that adding an antidepressant to electroconvulsive therapy (ECT), compared with ECT monotherapy, improves outcomes. We aimed to determine whether the addition of Nortriptyline to ECT enhances its efficacy and prevents post-ECT relapse. Methods: We conducted a randomized, double-blind, placebo-controlled trial (RCT). Patients with major depressive disorder and an indication for ECT received either Nortriptyline or placebo during a bilateral ECT course. Outcome measures were mean decrease in Hamilton Rating Scale for Depression (HRSD) score, response, remission, and time to response and remission. Patients who attained remission participated in a 1-year follow-up study with open-label Nortriptyline. Outcome measures were relapse and time to relapse. Results: We included 47 patients in the RCT. In the Nortriptyline group, 83% showed response, 74% attained remission, and the mean decrease in HRSD score was 21.6 points. In the placebo group these figures were, respectively, 81% (p = 0.945), 73% (p = 0.928) and 20.7 points (p = 0.748). Thirty-one patients participated in the follow-up study. In patients who had received Nortriptyline during the RCT, 47% relapsed at a mean of 34.2 weeks. Patients who had received placebo showed similar treatment results. In both study phases, no statistically significant differences between the Nortriptyline and the placebo group were found. Conclusion: In our sample of severely depressed patients who were often medication resistant and suffering from psychotic depression, the addition of Nortriptyline to ECT did not enhance its efficacy or prevent post-ECT relapse. Encouragingly, even in these patients ECT was highly effective and relapse rates were relatively low.