Osavampator

updated

Osavampator (TAK-653, also coded NBI-1065845) is an unapproved AMPA receptor potentiator with five phase 3 registrations recruiting for adjunctive use in major depressive disorder. No efficacy result in patients is public: the treatment-resistant depression phase 2 was withdrawn with 0 enrolled, and the 183-person phase 2 in major depressive disorder has no posted or published results. Human data are limited to healthy-volunteer target-engagement and interaction studies.

AMPA receptor positive modulator (potentiator)

  • TAK-653 is osavampator (INN): PubChem CID 56655833, C19H23N3O3S, 373.5 g/mol, CAS 1358751-06-0; the same record covers the code NBI-1065845.
  • An openFDA Drugs@FDA query for osavampator returned no application on 9 October 2026.
  • In 24 healthy volunteers, TAK-653 0.5 mg and 6 mg increased motor-evoked potential amplitude after transcranial magnetic stimulation.
  • NCT03312894, a phase 2 study in treatment-resistant depression, is withdrawn with enrollment 0; NCT05203341, a phase 2 in major depressive disorder (enrollment 183), is completed with no posted results.
  • Five phase 3 registrations for adjunctive use in major depressive disorder are recruiting, none with results.
  • The rat and monkey antidepressant-like effects followed 6 days and 2 weeks of dosing, so no study shows a rapid single-dose effect.

What is osavampator, and is it approved?

Osavampator is the INN for TAK-653, also coded NBI-1065845, an investigational AMPA receptor potentiator with no FDA approval record. An openFDA query for osavampator returned no application on 9 October 2026.

TAK-653 is osavampator (INN): PubChem CID 56655833, C19H23N3O3S, 373.5 g/mol, CAS 1358751-06-0. PubChem returns the same record for NBI-1065845, the code used in the phase 2 and phase 3 registrations, and a 2024 phase 1 report by Neurocrine Biosciences employees names the compound NBI-1065845 (TAK-653).

An openFDA Drugs@FDA query for osavampator returned no application on 9 October 2026. That is a dated, US-scoped search, and approvals outside the United States are not covered here. A ClinicalTrials.gov search for osavampator returned no records, because registrations use TAK-653 or NBI-1065845.

PubChem: osavampator (TAK-653, NBI-1065845) identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 56655833 (osavampator, TAK-653, NBI-1065845).

TAK-653 is osavampator (INN): PubChem CID 56655833, C19H23N3O3S, 373.5 g/mol, CAS 1358751-06-0. PubChem returns the same record for NBI-1065845, the code used in the phase 2 and phase 3 registrations, and a 2024 phase 1 report by Neurocrine Biosciences employees names the compound NBI-1065845 (TAK-653).

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Identity record only; it says nothing about efficacy or safety.

Read the original source
FDA record search, 9 October 2026: no matching application

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA API query run on 9 October 2026 for osavampator by brand or generic name, with a ClinicalTrials.gov search for osavampator on the same date.

The openFDA query for osavampator returned no application. No US approval record was found. A ClinicalTrials.gov search for osavampator returned no records, because registrations use TAK-653 or NBI-1065845. This supports only a dated, US-scoped statement.

Participants / model
FDA application database, not a clinical population
Treatment
Name search
Follow-up
Query run on 9 October 2026
Study design
Dated US approval-record search
Funding
not stated in the source

A search result shows what the database returned on that date. It is not a worldwide status claim.

Read the original source

What did the healthy-volunteer trials find?

In 24 healthy volunteers, TAK-653 increased the motor-evoked potential on transcranial magnetic stimulation and gave a psychostimulant-like profile on acute laboratory tests. These show target engagement, not an antidepressant or cognitive benefit in patients.

In 24 healthy volunteers (23 men, 1 woman), TAK-653 0.5 mg and 6 mg versus placebo in a double-blind crossover increased motor-evoked potential amplitude after single-pulse transcranial magnetic stimulation, without changing resting motor threshold or paired-pulse responses. In 31 rats, TAK-653 increased the corresponding response at similar plasma concentrations. The registry lists a completed 24-participant TMS study (NCT03792672) with results posted; the paper's abstract gives no registration number, and those posted results are not reported here.

In a randomized, double-blind, three-way crossover in 24 healthy volunteers (placebo, 0.5 mg, 6 mg), TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

In a drug interaction study in healthy adults (14 men and 4 women in the midazolam arm, 16 completed; 17 women in the oral contraceptive arm, 16 completed), geometric mean ratios for Cmax after multiple daily doses of NBI-1065845 were 0.94 (90% CI 0.79 to 1.13) for midazolam, 1.00 (0.87 to 1.15) for ethinyl estradiol and 0.99 (0.87 to 1.13) for levonorgestrel. AUC ratios were 0.88 (0.78 to 0.98) for midazolam, 1.01 (0.88 to 1.15) for ethinyl estradiol and 0.87 (0.78 to 0.96, to the last quantifiable concentration) for levonorgestrel. The authors conclude it is not a CYP3A inducer.

Target engagement: 24 volunteers, larger motor-evoked potentials

Randomized controlled trial

O'Donnell P et al. Transl Psychiatry. 2021;11(1):325. PMID 34045439.

TAK-653 0.5 mg and 6 mg versus placebo in a double-blind crossover increased motor-evoked potential amplitude after single-pulse transcranial magnetic stimulation, without changing resting motor threshold or paired-pulse responses. In 31 rats, TAK-653 increased the corresponding response at similar plasma concentrations.

Participants / model
24 healthy volunteers (23 men, 1 woman); 31 adult male rats
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract); rats 0.1 to 50 mg/kg
Follow-up
not stated in the source
Study design
Randomized double-blind crossover study with a rat arm
Funding
not stated in the source

Developer authors. The registry lists a completed 24-participant TMS study (NCT03792672) with results posted; the abstract gives no registration number, and those posted results are not reported here.

Read the original source
NeuroCart: 24 volunteers, acute tests, psychostimulant-like profile

Randomized controlled trial

Dijkstra F et al. Transl Psychiatry. 2022;12(1):408. PMID 36153330.

TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like.

Participants / model
24 healthy volunteers
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Randomized, double-blind, three-way crossover with the NeuroCart battery: body sway, eye movements, adaptive tracking, visual analogue scales and Stroop
Funding
not stated in the source

Developer co-authors. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

Read the original source
Interaction study: not a CYP3A inducer, 18 and 17 healthy adults

Clinical trial

Lin S et al. Clin Transl Sci. 2024;17(5):e13791. PMID 38700236.

After multiple daily doses of NBI-1065845, geometric mean ratios for Cmax were 0.94 (90% CI 0.79 to 1.13) for midazolam, 1.00 (0.87 to 1.15) for ethinyl estradiol, and 0.99 (0.87 to 1.13) for levonorgestrel; AUC ratios were 0.88 (0.78 to 0.98) for midazolam, 1.01 (0.88 to 1.15) for ethinyl estradiol, and 0.87 (0.78 to 0.96, to the last quantifiable concentration) for levonorgestrel. The authors conclude it is not a CYP3A inducer, and it was generally well tolerated. The report describes the compound as in phase 2 development for major depressive disorder at that time.

Participants / model
Healthy adults: 14 men and 4 women in the midazolam arm (16 completed); 17 women in the oral contraceptive arm (16 completed)
Treatment
NBI-1065845 multiple daily doses (route and dose not stated in the abstract) with midazolam or ethinyl estradiol-levonorgestrel
Follow-up
not stated in the source
Study design
Phase 1 probe-drug PK and safety study
Funding
not stated in the source

Developer authors (Neurocrine Biosciences employees).

Read the original source

Has osavampator been tested in depression, and what do the registrations show?

The treatment-resistant depression phase 2 was withdrawn with 0 enrolled, and the 183-person phase 2 in major depressive disorder is completed without posted or published results. Five phase 3 studies in major depressive disorder are recruiting.

NCT03312894, a phase 2 study of TAK-653 in treatment-resistant depression, is listed as withdrawn with enrollment 0. No other TAK-653 or NBI-1065845 registration returned on 9 October 2026 names treatment-resistant depression in its title.

NCT05203341, a phase 2 study of NBI-1065845 in adults with major depressive disorder, is listed as completed with enrollment 183 and no posted results, and no PubMed report of it was found on 9 October 2026. A completed registration is not evidence of efficacy.

Phase 3 is under way as adjunctive treatment for major depressive disorder, with all five registrations recruiting and none with results: three efficacy and safety studies (NCT06786624, NCT06911112 and NCT06963021, enrollment 200 each), a long-term safety and tolerability study (NCT06966401, enrollment 850), and a maintenance study (NCT07196501, enrollment 550). No dose for the phase 2 or phase 3 program appears in the sources reviewed.

A completed phase 1 single and multiple ascending dose study in healthy participants (NCT02561156, enrollment 88) has results posted, but no PubMed report of it was found and its posted results are not reported here.

Registry: treatment-resistant depression phase 2, withdrawn, enrollment 0

Trial registry record

ClinicalTrials.gov. NCT03312894, phase 2 study of TAK-653 in treatment-resistant depression.

NCT03312894, a phase 2 study of TAK-653 in treatment-resistant depression, is listed as withdrawn with enrollment 0. No other TAK-653 or NBI-1065845 registration returned on 9 October 2026 names treatment-resistant depression in its title.

Participants / model
Registry record, not a population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No participant was enrolled, so this registration has no result of any kind.

Read the original source
Registry: phase 2 in major depressive disorder, completed, enrollment 183, no results

Trial registry record

ClinicalTrials.gov. NCT05203341, phase 2 study of NBI-1065845 in adults with major depressive disorder.

NCT05203341, a phase 2 study of NBI-1065845 in adults with major depressive disorder, is listed as completed with enrollment 183 and no posted results, and no PubMed report of it was found on 9 October 2026.

Participants / model
Adults with major depressive disorder (registry description)
Treatment
NBI-1065845 (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

A completed registration is not evidence of efficacy.

Read the original source
Registry: five phase 3 registrations, all recruiting, none with results

Trial registry record

ClinicalTrials.gov. NCT06786624, with related phase 3 records NCT06911112, NCT06963021, NCT06966401 and NCT07196501.

Phase 3 is under way as adjunctive treatment for major depressive disorder, with all five registrations recruiting and none with results: three efficacy and safety studies (NCT06786624, NCT06911112 and NCT06963021, enrollment 200 each), a long-term safety and tolerability study (NCT06966401, enrollment 850), and a maintenance study (NCT07196501, enrollment 550).

Participants / model
Participants with major depressive disorder (registry descriptions)
Treatment
NBI-1065845 as adjunctive treatment (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No dose for the phase 2 or phase 3 program appears in the sources reviewed.

Read the original source
Registry: phase 1 ascending dose study, 88 participants, results posted

Trial registry record

ClinicalTrials.gov. NCT02561156, phase 1 single and multiple ascending dose study of TAK-653 in healthy participants.

ClinicalTrials.gov lists a completed phase 1 single and multiple ascending dose study of TAK-653 in healthy participants (NCT02561156, enrollment 88) with results posted. No PubMed report of this study was found, and its posted safety and PK results are not reported here.

Participants / model
Healthy participants (registry description)
Treatment
TAK-653 single and multiple doses (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

Posted registry results exist but are not summarized on this page, so no adverse-event rate or half-life is given from them.

Read the original source

What do the cell and animal studies show?

In cells, rats and monkeys, TAK-653 potentiated AMPA receptors, raised BDNF and produced antidepressant-like or motivation-related effects after 6 days to 2 weeks of dosing. None of these showed a rapid single-dose effect.

TAK-653 is an AMPA receptor potentiator with minimal agonist activity. It bound the receptor's ligand-binding domain in a glutamate-dependent way, potentiated glutamate-induced calcium influx, and enhanced evoked AMPA receptor-mediated synaptic potentials in brain slices more potently than AMPA or LY451646, a potentiator with prominent agonist activity. It improved working memory and recognition memory in animal tests (species not stated in the abstract).

In rat primary cortical neurons, TAK-653 increased phosphorylated mTOR, p70S6 kinase, Akt and ERK and raised BDNF protein. Six days of sub-chronic dosing produced an antidepressant-like effect in the rat reduction of submissive behavior model, where ketamine's effect was blocked by an AMPA receptor antagonist. Unlike ketamine, TAK-653 did not cause hyperlocomotion. Because the effect followed 6 days of dosing, this study does not show a rapid, single-dose effect.

In monkeys after 12 weeks of chronic unpredictable mild stress, two weeks of TAK-653 improved motivation for food, reduced huddling, increased activity and time in the upper enclosure, lowered plasma cortisol and IL-6, and raised BDNF expression. The abstract gives neither the number of animals nor the dose, and the authors report no conflicts of interest.

Preclinical: AMPA potentiator, memory tests, convulsion margin 419-fold

Animal study

Suzuki A et al. Sci Rep. 2021;11(1):14532. PMID 34267258.

TAK-653 is an AMPA receptor potentiator with minimal agonist activity. It bound the receptor's ligand-binding domain in a glutamate-dependent way, potentiated glutamate-induced calcium influx, and enhanced evoked AMPA receptor-mediated synaptic potentials in brain slices more potently than AMPA or LY451646, a potentiator with prominent agonist activity. It improved working memory and recognition memory in animal tests (species not stated in the abstract), and its convulsion safety margin in rats was 419-fold by plasma Cmax and 1017-fold by AUC.

Participants / model
Recombinant receptors in CHO cells, primary neurons, brain slices; animals for memory tests; rats for convulsion margin
Treatment
In vitro; in vivo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Preclinical study of receptor binding, calcium influx, synaptic potentials, memory tasks and convulsion margin
Funding
not stated in the source

Developer authors. The abstract does not give the species for the memory tests, or the route and dose.

Read the original source
Rats: mTOR, Akt, ERK and BDNF; effect after 6 days of dosing

Animal study

Hara H et al. Pharmacol Biochem Behav. 2021;211:173289. PMID 34655652.

In rat primary cortical neurons, TAK-653 increased phosphorylated mTOR, p70S6 kinase, Akt, and ERK and raised BDNF protein. Six days of sub-chronic dosing produced an antidepressant-like effect in the rat reduction of submissive behavior model, where ketamine's effect was blocked by an AMPA receptor antagonist. Unlike ketamine, TAK-653 did not cause hyperlocomotion.

Participants / model
Rats; rat primary cortical neurons
Treatment
Sub-chronic dosing for 6 days (route not stated in the abstract)
Follow-up
6 days of dosing
Study design
Preclinical study of signaling proteins, BDNF, submissive behavior and locomotion
Funding
not stated in the source

Developer authors. Because the effect followed 6 days of dosing, this study does not show a rapid, single-dose effect.

Read the original source
Monkeys after 12 weeks of stress: 2 weeks of TAK-653

Animal study

Li L et al. Biomedicines. 2025;13(6). PMID 40564108.

In monkeys after 12 weeks of chronic unpredictable mild stress, two weeks of TAK-653 improved motivation for food, reduced huddling, increased activity and time in the upper enclosure, lowered plasma cortisol and IL-6, and raised BDNF expression.

Participants / model
Monkeys with chronic stress-induced depression-like behavior
Treatment
TAK-653 for 2 weeks (route and dose not stated in the abstract)
Follow-up
2 weeks of treatment after 12 weeks of stress
Study design
Preclinical study of behavior, plasma cortisol, IL-6 and BDNF
Funding
not stated in the source

The abstract gives neither the number of animals nor the dose. The authors report no conflicts of interest.

Read the original source

Does osavampator treat treatment-resistant depression, work rapidly, or enhance cognition?

AMPA potentiation is the correct mechanism, but no trial in treatment-resistant depression enrolled anyone, no human data show a rapid effect, and the cognition claim rests on acute laboratory tasks in healthy volunteers and animal memory tests.

Sellers describe osavampator as treating treatment-resistant depression, giving rapid antidepressant effects, and enhancing cognition through AMPA receptor potentiation.

On the mechanism, AMPA potentiation is correct. On treatment-resistant depression, the one phase 2 registration (NCT03312894) was withdrawn with enrollment 0, so no trial in that population enrolled anyone.

On speed of onset, there are no human data. The rat antidepressant-like effect followed 6 days of dosing and the monkey effect followed 2 weeks of dosing.

On cognition, the human findings are acute NeuroCart laboratory tasks in 24 healthy volunteers, and the other support is animal memory tests. A PubMed search on 9 October 2026 for TAK-653, TAK653, "TAK 653", osavampator, NBI-1065845 or NBI1065845 returned 12 records, and none reports antidepressant efficacy, speed of onset or a cognitive outcome in patients with depression of any kind.

PubMed search, 9 October 2026: 12 records, none reporting efficacy in patients

PubMed search record

PubMed search run on 9 October 2026: TAK-653 OR TAK653 OR "TAK 653" OR osavampator OR NBI-1065845 OR NBI1065845. 12 records returned.

The search returned 12 records: 3 human studies in healthy volunteers, 2 developer preclinical reports and 1 independent monkey study, 1 author correction, and 5 reviews. None reports antidepressant efficacy, speed of onset, or a cognitive outcome in patients with depression of any kind.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Search run on 9 October 2026
Study design
Literature search
Funding
not stated in the source

A search result shows what PubMed returned on that date. It is not proof that no unindexed study exists.

Read the original source
Registry: treatment-resistant depression phase 2, withdrawn, enrollment 0

Trial registry record

ClinicalTrials.gov. NCT03312894, phase 2 study of TAK-653 in treatment-resistant depression.

NCT03312894, a phase 2 study of TAK-653 in treatment-resistant depression, is listed as withdrawn with enrollment 0. No other TAK-653 or NBI-1065845 registration returned on 9 October 2026 names treatment-resistant depression in its title.

Participants / model
Registry record, not a population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No participant was enrolled, so this registration has no result of any kind.

Read the original source
NeuroCart: 24 volunteers, acute tests, psychostimulant-like profile

Randomized controlled trial

Dijkstra F et al. Transl Psychiatry. 2022;12(1):408. PMID 36153330.

TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like.

Participants / model
24 healthy volunteers
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Randomized, double-blind, three-way crossover with the NeuroCart battery: body sway, eye movements, adaptive tracking, visual analogue scales and Stroop
Funding
not stated in the source

Developer co-authors. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

Read the original source
Rats: mTOR, Akt, ERK and BDNF; effect after 6 days of dosing

Animal study

Hara H et al. Pharmacol Biochem Behav. 2021;211:173289. PMID 34655652.

In rat primary cortical neurons, TAK-653 increased phosphorylated mTOR, p70S6 kinase, Akt, and ERK and raised BDNF protein. Six days of sub-chronic dosing produced an antidepressant-like effect in the rat reduction of submissive behavior model, where ketamine's effect was blocked by an AMPA receptor antagonist. Unlike ketamine, TAK-653 did not cause hyperlocomotion.

Participants / model
Rats; rat primary cortical neurons
Treatment
Sub-chronic dosing for 6 days (route not stated in the abstract)
Follow-up
6 days of dosing
Study design
Preclinical study of signaling proteins, BDNF, submissive behavior and locomotion
Funding
not stated in the source

Developer authors. Because the effect followed 6 days of dosing, this study does not show a rapid, single-dose effect.

Read the original source
Monkeys after 12 weeks of stress: 2 weeks of TAK-653

Animal study

Li L et al. Biomedicines. 2025;13(6). PMID 40564108.

In monkeys after 12 weeks of chronic unpredictable mild stress, two weeks of TAK-653 improved motivation for food, reduced huddling, increased activity and time in the upper enclosure, lowered plasma cortisol and IL-6, and raised BDNF expression.

Participants / model
Monkeys with chronic stress-induced depression-like behavior
Treatment
TAK-653 for 2 weeks (route and dose not stated in the abstract)
Follow-up
2 weeks of treatment after 12 weeks of stress
Study design
Preclinical study of behavior, plasma cortisol, IL-6 and BDNF
Funding
not stated in the source

The abstract gives neither the number of animals nor the dose. The authors report no conflicts of interest.

Read the original source

How does osavampator work, and what does the body do with it?

Osavampator is an AMPA receptor potentiator with minimal agonist activity. No half-life or Tmax is given here, and an interaction study found it is not a CYP3A inducer.

TAK-653 binds the AMPA receptor's ligand-binding domain in a glutamate-dependent way and potentiates glutamate-induced calcium influx, with minimal agonist activity of its own. In rat neurons it increased phosphorylated mTOR, p70S6 kinase, Akt and ERK and raised BDNF protein. The TMS study in healthy volunteers is the human target-engagement result: motor-evoked potential amplitude rose without a change in resting motor threshold or paired-pulse responses.

In the interaction study in healthy adults, geometric mean ratios were close to 1 for ethinyl estradiol and levonorgestrel Cmax and for ethinyl estradiol AUC, and AUC ratios were 0.88 for midazolam and 0.87 for levonorgestrel. The authors conclude it is not a CYP3A inducer.

A half-life and Tmax are not given on this page. The phase 1 ascending dose study (NCT02561156) has posted registry results that are not reported here, and the abstracts of the other human studies do not state them.

Preclinical: AMPA potentiator, memory tests, convulsion margin 419-fold

Animal study

Suzuki A et al. Sci Rep. 2021;11(1):14532. PMID 34267258.

TAK-653 is an AMPA receptor potentiator with minimal agonist activity. It bound the receptor's ligand-binding domain in a glutamate-dependent way, potentiated glutamate-induced calcium influx, and enhanced evoked AMPA receptor-mediated synaptic potentials in brain slices more potently than AMPA or LY451646, a potentiator with prominent agonist activity. It improved working memory and recognition memory in animal tests (species not stated in the abstract), and its convulsion safety margin in rats was 419-fold by plasma Cmax and 1017-fold by AUC.

Participants / model
Recombinant receptors in CHO cells, primary neurons, brain slices; animals for memory tests; rats for convulsion margin
Treatment
In vitro; in vivo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Preclinical study of receptor binding, calcium influx, synaptic potentials, memory tasks and convulsion margin
Funding
not stated in the source

Developer authors. The abstract does not give the species for the memory tests, or the route and dose.

Read the original source
Rats: mTOR, Akt, ERK and BDNF; effect after 6 days of dosing

Animal study

Hara H et al. Pharmacol Biochem Behav. 2021;211:173289. PMID 34655652.

In rat primary cortical neurons, TAK-653 increased phosphorylated mTOR, p70S6 kinase, Akt, and ERK and raised BDNF protein. Six days of sub-chronic dosing produced an antidepressant-like effect in the rat reduction of submissive behavior model, where ketamine's effect was blocked by an AMPA receptor antagonist. Unlike ketamine, TAK-653 did not cause hyperlocomotion.

Participants / model
Rats; rat primary cortical neurons
Treatment
Sub-chronic dosing for 6 days (route not stated in the abstract)
Follow-up
6 days of dosing
Study design
Preclinical study of signaling proteins, BDNF, submissive behavior and locomotion
Funding
not stated in the source

Developer authors. Because the effect followed 6 days of dosing, this study does not show a rapid, single-dose effect.

Read the original source
Target engagement: 24 volunteers, larger motor-evoked potentials

Randomized controlled trial

O'Donnell P et al. Transl Psychiatry. 2021;11(1):325. PMID 34045439.

TAK-653 0.5 mg and 6 mg versus placebo in a double-blind crossover increased motor-evoked potential amplitude after single-pulse transcranial magnetic stimulation, without changing resting motor threshold or paired-pulse responses. In 31 rats, TAK-653 increased the corresponding response at similar plasma concentrations.

Participants / model
24 healthy volunteers (23 men, 1 woman); 31 adult male rats
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract); rats 0.1 to 50 mg/kg
Follow-up
not stated in the source
Study design
Randomized double-blind crossover study with a rat arm
Funding
not stated in the source

Developer authors. The registry lists a completed 24-participant TMS study (NCT03792672) with results posted; the abstract gives no registration number, and those posted results are not reported here.

Read the original source
Interaction study: not a CYP3A inducer, 18 and 17 healthy adults

Clinical trial

Lin S et al. Clin Transl Sci. 2024;17(5):e13791. PMID 38700236.

After multiple daily doses of NBI-1065845, geometric mean ratios for Cmax were 0.94 (90% CI 0.79 to 1.13) for midazolam, 1.00 (0.87 to 1.15) for ethinyl estradiol, and 0.99 (0.87 to 1.13) for levonorgestrel; AUC ratios were 0.88 (0.78 to 0.98) for midazolam, 1.01 (0.88 to 1.15) for ethinyl estradiol, and 0.87 (0.78 to 0.96, to the last quantifiable concentration) for levonorgestrel. The authors conclude it is not a CYP3A inducer, and it was generally well tolerated. The report describes the compound as in phase 2 development for major depressive disorder at that time.

Participants / model
Healthy adults: 14 men and 4 women in the midazolam arm (16 completed); 17 women in the oral contraceptive arm (16 completed)
Treatment
NBI-1065845 multiple daily doses (route and dose not stated in the abstract) with midazolam or ethinyl estradiol-levonorgestrel
Follow-up
not stated in the source
Study design
Phase 1 probe-drug PK and safety study
Funding
not stated in the source

Developer authors (Neurocrine Biosciences employees).

Read the original source
Registry: phase 1 ascending dose study, 88 participants, results posted

Trial registry record

ClinicalTrials.gov. NCT02561156, phase 1 single and multiple ascending dose study of TAK-653 in healthy participants.

ClinicalTrials.gov lists a completed phase 1 single and multiple ascending dose study of TAK-653 in healthy participants (NCT02561156, enrollment 88) with results posted. No PubMed report of this study was found, and its posted safety and PK results are not reported here.

Participants / model
Healthy participants (registry description)
Treatment
TAK-653 single and multiple doses (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

Posted registry results exist but are not summarized on this page, so no adverse-event rate or half-life is given from them.

Read the original source

What risks did the studies report?

In healthy adults, the interaction study found NBI-1065845 generally well tolerated, and TAK-653 did not change body sway or subjective drug effects. No adverse-event rate is given here, and the rat convulsion safety margin was 419-fold by plasma Cmax.

In rats, the convulsion safety margin was 419-fold by plasma Cmax and 1017-fold by AUC. In healthy adults, NBI-1065845 was generally well tolerated in the interaction study, and TAK-653 did not change body sway or subjective drug effects in the NeuroCart study.

No adverse-event rate is given on this page. Posted registry results for the 88-participant phase 1 study (NCT02561156) and the 24-participant TMS study (NCT03792672) are not reported here, and none of the phase 3 studies has results. No dose for the phase 2 or phase 3 program appears in the sources reviewed.

The authors of the NeuroCart study describe the profile as psychostimulant-like. No safety information exists for the supplier uses in treatment-resistant depression or for cognitive enhancement.

Preclinical: AMPA potentiator, memory tests, convulsion margin 419-fold

Animal study

Suzuki A et al. Sci Rep. 2021;11(1):14532. PMID 34267258.

TAK-653 is an AMPA receptor potentiator with minimal agonist activity. It bound the receptor's ligand-binding domain in a glutamate-dependent way, potentiated glutamate-induced calcium influx, and enhanced evoked AMPA receptor-mediated synaptic potentials in brain slices more potently than AMPA or LY451646, a potentiator with prominent agonist activity. It improved working memory and recognition memory in animal tests (species not stated in the abstract), and its convulsion safety margin in rats was 419-fold by plasma Cmax and 1017-fold by AUC.

Participants / model
Recombinant receptors in CHO cells, primary neurons, brain slices; animals for memory tests; rats for convulsion margin
Treatment
In vitro; in vivo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Preclinical study of receptor binding, calcium influx, synaptic potentials, memory tasks and convulsion margin
Funding
not stated in the source

Developer authors. The abstract does not give the species for the memory tests, or the route and dose.

Read the original source
Interaction study: not a CYP3A inducer, 18 and 17 healthy adults

Clinical trial

Lin S et al. Clin Transl Sci. 2024;17(5):e13791. PMID 38700236.

After multiple daily doses of NBI-1065845, geometric mean ratios for Cmax were 0.94 (90% CI 0.79 to 1.13) for midazolam, 1.00 (0.87 to 1.15) for ethinyl estradiol, and 0.99 (0.87 to 1.13) for levonorgestrel; AUC ratios were 0.88 (0.78 to 0.98) for midazolam, 1.01 (0.88 to 1.15) for ethinyl estradiol, and 0.87 (0.78 to 0.96, to the last quantifiable concentration) for levonorgestrel. The authors conclude it is not a CYP3A inducer, and it was generally well tolerated. The report describes the compound as in phase 2 development for major depressive disorder at that time.

Participants / model
Healthy adults: 14 men and 4 women in the midazolam arm (16 completed); 17 women in the oral contraceptive arm (16 completed)
Treatment
NBI-1065845 multiple daily doses (route and dose not stated in the abstract) with midazolam or ethinyl estradiol-levonorgestrel
Follow-up
not stated in the source
Study design
Phase 1 probe-drug PK and safety study
Funding
not stated in the source

Developer authors (Neurocrine Biosciences employees).

Read the original source
NeuroCart: 24 volunteers, acute tests, psychostimulant-like profile

Randomized controlled trial

Dijkstra F et al. Transl Psychiatry. 2022;12(1):408. PMID 36153330.

TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like.

Participants / model
24 healthy volunteers
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Randomized, double-blind, three-way crossover with the NeuroCart battery: body sway, eye movements, adaptive tracking, visual analogue scales and Stroop
Funding
not stated in the source

Developer co-authors. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

Read the original source
Registry: phase 1 ascending dose study, 88 participants, results posted

Trial registry record

ClinicalTrials.gov. NCT02561156, phase 1 single and multiple ascending dose study of TAK-653 in healthy participants.

ClinicalTrials.gov lists a completed phase 1 single and multiple ascending dose study of TAK-653 in healthy participants (NCT02561156, enrollment 88) with results posted. No PubMed report of this study was found, and its posted safety and PK results are not reported here.

Participants / model
Healthy participants (registry description)
Treatment
TAK-653 single and multiple doses (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

Posted registry results exist but are not summarized on this page, so no adverse-event rate or half-life is given from them.

Read the original source

Why does osavampator sit in C tier?

Osavampator has well-characterized pharmacology, human target engagement in two 24-person studies and five recruiting phase 3 registrations. No efficacy result in patients is public, so the grade does not cover the supplier's treatment-resistant depression, rapid-onset or cognition claims.

The C reflects well-characterized pharmacology, human target engagement in two 24-person healthy-volunteer studies (a larger motor-evoked potential on TMS and a stimulant-like NeuroCart profile), and five phase 3 registrations for adjunctive use in major depressive disorder that are recruiting.

But no efficacy result in patients is public. The treatment-resistant depression phase 2 was withdrawn before enrolling, and the 183-person phase 2 in major depressive disorder is completed without posted or published results.

On the supplier's claims, AMPA potentiation is the correct mechanism, treatment-resistant depression has no trial that enrolled anyone, a rapid antidepressant effect has no human data and the animal effects followed 6 days (rats) and 2 weeks (monkeys) of dosing, and the cognition claim rests on acute laboratory tasks in healthy volunteers and animal memory tests.

Target engagement: 24 volunteers, larger motor-evoked potentials

Randomized controlled trial

O'Donnell P et al. Transl Psychiatry. 2021;11(1):325. PMID 34045439.

TAK-653 0.5 mg and 6 mg versus placebo in a double-blind crossover increased motor-evoked potential amplitude after single-pulse transcranial magnetic stimulation, without changing resting motor threshold or paired-pulse responses. In 31 rats, TAK-653 increased the corresponding response at similar plasma concentrations.

Participants / model
24 healthy volunteers (23 men, 1 woman); 31 adult male rats
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract); rats 0.1 to 50 mg/kg
Follow-up
not stated in the source
Study design
Randomized double-blind crossover study with a rat arm
Funding
not stated in the source

Developer authors. The registry lists a completed 24-participant TMS study (NCT03792672) with results posted; the abstract gives no registration number, and those posted results are not reported here.

Read the original source
NeuroCart: 24 volunteers, acute tests, psychostimulant-like profile

Randomized controlled trial

Dijkstra F et al. Transl Psychiatry. 2022;12(1):408. PMID 36153330.

TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like.

Participants / model
24 healthy volunteers
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Randomized, double-blind, three-way crossover with the NeuroCart battery: body sway, eye movements, adaptive tracking, visual analogue scales and Stroop
Funding
not stated in the source

Developer co-authors. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

Read the original source
Registry: five phase 3 registrations, all recruiting, none with results

Trial registry record

ClinicalTrials.gov. NCT06786624, with related phase 3 records NCT06911112, NCT06963021, NCT06966401 and NCT07196501.

Phase 3 is under way as adjunctive treatment for major depressive disorder, with all five registrations recruiting and none with results: three efficacy and safety studies (NCT06786624, NCT06911112 and NCT06963021, enrollment 200 each), a long-term safety and tolerability study (NCT06966401, enrollment 850), and a maintenance study (NCT07196501, enrollment 550).

Participants / model
Participants with major depressive disorder (registry descriptions)
Treatment
NBI-1065845 as adjunctive treatment (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No dose for the phase 2 or phase 3 program appears in the sources reviewed.

Read the original source
Registry: treatment-resistant depression phase 2, withdrawn, enrollment 0

Trial registry record

ClinicalTrials.gov. NCT03312894, phase 2 study of TAK-653 in treatment-resistant depression.

NCT03312894, a phase 2 study of TAK-653 in treatment-resistant depression, is listed as withdrawn with enrollment 0. No other TAK-653 or NBI-1065845 registration returned on 9 October 2026 names treatment-resistant depression in its title.

Participants / model
Registry record, not a population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No participant was enrolled, so this registration has no result of any kind.

Read the original source
Registry: phase 2 in major depressive disorder, completed, enrollment 183, no results

Trial registry record

ClinicalTrials.gov. NCT05203341, phase 2 study of NBI-1065845 in adults with major depressive disorder.

NCT05203341, a phase 2 study of NBI-1065845 in adults with major depressive disorder, is listed as completed with enrollment 183 and no posted results, and no PubMed report of it was found on 9 October 2026.

Participants / model
Adults with major depressive disorder (registry description)
Treatment
NBI-1065845 (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

A completed registration is not evidence of efficacy.

Read the original source
PubMed search, 9 October 2026: 12 records, none reporting efficacy in patients

PubMed search record

PubMed search run on 9 October 2026: TAK-653 OR TAK653 OR "TAK 653" OR osavampator OR NBI-1065845 OR NBI1065845. 12 records returned.

The search returned 12 records: 3 human studies in healthy volunteers, 2 developer preclinical reports and 1 independent monkey study, 1 author correction, and 5 reviews. None reports antidepressant efficacy, speed of onset, or a cognitive outcome in patients with depression of any kind.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Search run on 9 October 2026
Study design
Literature search
Funding
not stated in the source

A search result shows what PubMed returned on that date. It is not proof that no unindexed study exists.

Read the original source

Studies and sources

PubChem: osavampator (TAK-653, NBI-1065845) identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 56655833 (osavampator, TAK-653, NBI-1065845).

TAK-653 is osavampator (INN): PubChem CID 56655833, C19H23N3O3S, 373.5 g/mol, CAS 1358751-06-0. PubChem returns the same record for NBI-1065845, the code used in the phase 2 and phase 3 registrations, and a 2024 phase 1 report by Neurocrine Biosciences employees names the compound NBI-1065845 (TAK-653).

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Identity record only; it says nothing about efficacy or safety.

Read the original source
Preclinical: AMPA potentiator, memory tests, convulsion margin 419-fold

Animal study

Suzuki A et al. Sci Rep. 2021;11(1):14532. PMID 34267258.

TAK-653 is an AMPA receptor potentiator with minimal agonist activity. It bound the receptor's ligand-binding domain in a glutamate-dependent way, potentiated glutamate-induced calcium influx, and enhanced evoked AMPA receptor-mediated synaptic potentials in brain slices more potently than AMPA or LY451646, a potentiator with prominent agonist activity. It improved working memory and recognition memory in animal tests (species not stated in the abstract), and its convulsion safety margin in rats was 419-fold by plasma Cmax and 1017-fold by AUC.

Participants / model
Recombinant receptors in CHO cells, primary neurons, brain slices; animals for memory tests; rats for convulsion margin
Treatment
In vitro; in vivo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Preclinical study of receptor binding, calcium influx, synaptic potentials, memory tasks and convulsion margin
Funding
not stated in the source

Developer authors. The abstract does not give the species for the memory tests, or the route and dose.

Read the original source
Rats: mTOR, Akt, ERK and BDNF; effect after 6 days of dosing

Animal study

Hara H et al. Pharmacol Biochem Behav. 2021;211:173289. PMID 34655652.

In rat primary cortical neurons, TAK-653 increased phosphorylated mTOR, p70S6 kinase, Akt, and ERK and raised BDNF protein. Six days of sub-chronic dosing produced an antidepressant-like effect in the rat reduction of submissive behavior model, where ketamine's effect was blocked by an AMPA receptor antagonist. Unlike ketamine, TAK-653 did not cause hyperlocomotion.

Participants / model
Rats; rat primary cortical neurons
Treatment
Sub-chronic dosing for 6 days (route not stated in the abstract)
Follow-up
6 days of dosing
Study design
Preclinical study of signaling proteins, BDNF, submissive behavior and locomotion
Funding
not stated in the source

Developer authors. Because the effect followed 6 days of dosing, this study does not show a rapid, single-dose effect.

Read the original source
Monkeys after 12 weeks of stress: 2 weeks of TAK-653

Animal study

Li L et al. Biomedicines. 2025;13(6). PMID 40564108.

In monkeys after 12 weeks of chronic unpredictable mild stress, two weeks of TAK-653 improved motivation for food, reduced huddling, increased activity and time in the upper enclosure, lowered plasma cortisol and IL-6, and raised BDNF expression.

Participants / model
Monkeys with chronic stress-induced depression-like behavior
Treatment
TAK-653 for 2 weeks (route and dose not stated in the abstract)
Follow-up
2 weeks of treatment after 12 weeks of stress
Study design
Preclinical study of behavior, plasma cortisol, IL-6 and BDNF
Funding
not stated in the source

The abstract gives neither the number of animals nor the dose. The authors report no conflicts of interest.

Read the original source
Target engagement: 24 volunteers, larger motor-evoked potentials

Randomized controlled trial

O'Donnell P et al. Transl Psychiatry. 2021;11(1):325. PMID 34045439.

TAK-653 0.5 mg and 6 mg versus placebo in a double-blind crossover increased motor-evoked potential amplitude after single-pulse transcranial magnetic stimulation, without changing resting motor threshold or paired-pulse responses. In 31 rats, TAK-653 increased the corresponding response at similar plasma concentrations.

Participants / model
24 healthy volunteers (23 men, 1 woman); 31 adult male rats
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract); rats 0.1 to 50 mg/kg
Follow-up
not stated in the source
Study design
Randomized double-blind crossover study with a rat arm
Funding
not stated in the source

Developer authors. The registry lists a completed 24-participant TMS study (NCT03792672) with results posted; the abstract gives no registration number, and those posted results are not reported here.

Read the original source
NeuroCart: 24 volunteers, acute tests, psychostimulant-like profile

Randomized controlled trial

Dijkstra F et al. Transl Psychiatry. 2022;12(1):408. PMID 36153330.

TAK-653 did not change body sway or subjective drug effects on visual analogue scales. At 6 mg it improved adaptive tracking (1.68%, interval 0.51 to 2.84, P=0.02) and increased smooth pursuit (2.32%, 0.37 to 4.27, P=0.05) and saccadic peak velocity (15.40 degrees per second, 1.91 to 28.90, P=0.06). At 0.5 mg it increased saccadic peak velocity (19.49 degrees per second, 5.98 to 32.99, P=0.02) and changed two Stroop measures (reaction-time difference 22.0, 4.0 to 40.0, P=0.05; correct incongruent responses -0.3, -0.5 to -0.1, P=0.02), which the abstract reports as effects rather than improvements. The authors call the profile psychostimulant-like.

Participants / model
24 healthy volunteers
Treatment
TAK-653 0.5 mg and 6 mg versus placebo (route not stated in the abstract)
Follow-up
not stated in the source
Study design
Randomized, double-blind, three-way crossover with the NeuroCart battery: body sway, eye movements, adaptive tracking, visual analogue scales and Stroop
Funding
not stated in the source

Developer co-authors. These are acute laboratory measures in healthy people, not cognitive enhancement over time or in patients.

Read the original source
Interaction study: not a CYP3A inducer, 18 and 17 healthy adults

Clinical trial

Lin S et al. Clin Transl Sci. 2024;17(5):e13791. PMID 38700236.

After multiple daily doses of NBI-1065845, geometric mean ratios for Cmax were 0.94 (90% CI 0.79 to 1.13) for midazolam, 1.00 (0.87 to 1.15) for ethinyl estradiol, and 0.99 (0.87 to 1.13) for levonorgestrel; AUC ratios were 0.88 (0.78 to 0.98) for midazolam, 1.01 (0.88 to 1.15) for ethinyl estradiol, and 0.87 (0.78 to 0.96, to the last quantifiable concentration) for levonorgestrel. The authors conclude it is not a CYP3A inducer, and it was generally well tolerated. The report describes the compound as in phase 2 development for major depressive disorder at that time.

Participants / model
Healthy adults: 14 men and 4 women in the midazolam arm (16 completed); 17 women in the oral contraceptive arm (16 completed)
Treatment
NBI-1065845 multiple daily doses (route and dose not stated in the abstract) with midazolam or ethinyl estradiol-levonorgestrel
Follow-up
not stated in the source
Study design
Phase 1 probe-drug PK and safety study
Funding
not stated in the source

Developer authors (Neurocrine Biosciences employees).

Read the original source
Registry: phase 1 ascending dose study, 88 participants, results posted

Trial registry record

ClinicalTrials.gov. NCT02561156, phase 1 single and multiple ascending dose study of TAK-653 in healthy participants.

ClinicalTrials.gov lists a completed phase 1 single and multiple ascending dose study of TAK-653 in healthy participants (NCT02561156, enrollment 88) with results posted. No PubMed report of this study was found, and its posted safety and PK results are not reported here.

Participants / model
Healthy participants (registry description)
Treatment
TAK-653 single and multiple doses (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

Posted registry results exist but are not summarized on this page, so no adverse-event rate or half-life is given from them.

Read the original source
Registry: treatment-resistant depression phase 2, withdrawn, enrollment 0

Trial registry record

ClinicalTrials.gov. NCT03312894, phase 2 study of TAK-653 in treatment-resistant depression.

NCT03312894, a phase 2 study of TAK-653 in treatment-resistant depression, is listed as withdrawn with enrollment 0. No other TAK-653 or NBI-1065845 registration returned on 9 October 2026 names treatment-resistant depression in its title.

Participants / model
Registry record, not a population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No participant was enrolled, so this registration has no result of any kind.

Read the original source
Registry: phase 2 in major depressive disorder, completed, enrollment 183, no results

Trial registry record

ClinicalTrials.gov. NCT05203341, phase 2 study of NBI-1065845 in adults with major depressive disorder.

NCT05203341, a phase 2 study of NBI-1065845 in adults with major depressive disorder, is listed as completed with enrollment 183 and no posted results, and no PubMed report of it was found on 9 October 2026.

Participants / model
Adults with major depressive disorder (registry description)
Treatment
NBI-1065845 (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

A completed registration is not evidence of efficacy.

Read the original source
Registry: five phase 3 registrations, all recruiting, none with results

Trial registry record

ClinicalTrials.gov. NCT06786624, with related phase 3 records NCT06911112, NCT06963021, NCT06966401 and NCT07196501.

Phase 3 is under way as adjunctive treatment for major depressive disorder, with all five registrations recruiting and none with results: three efficacy and safety studies (NCT06786624, NCT06911112 and NCT06963021, enrollment 200 each), a long-term safety and tolerability study (NCT06966401, enrollment 850), and a maintenance study (NCT07196501, enrollment 550).

Participants / model
Participants with major depressive disorder (registry descriptions)
Treatment
NBI-1065845 as adjunctive treatment (registry)
Follow-up
Not applicable
Study design
Official trial registry
Funding
not stated in the source

No dose for the phase 2 or phase 3 program appears in the sources reviewed.

Read the original source

Why is Osavampator in C tier?

C fits an AMPA potentiator with well-characterized pharmacology, human target engagement in two 24-person healthy-volunteer studies and five recruiting phase 3 registrations. No efficacy result in patients is public, the treatment-resistant depression phase 2 never enrolled anyone, and the 183-person phase 2 has no posted or published results. The grade does not cover the supplier's rapid-onset or cognition claims.