NSI-189 phosphate

updated

NSI-189 phosphate is an unapproved investigational compound that was tested for major depressive disorder. Its phase 2 trial in 220 outpatients missed the primary endpoint at both doses, and the neurogenesis and cognition findings come from cells and rodents. A PubMed search on 9 October 2026 for NSI-189 with trenbolone returned 0 records, so the recovery claim has no study behind it.

Investigational small molecule studied for neurogenesis in depression

  • openFDA Drugs@FDA queries for NSI-189 and for amdiglurax returned no application on 9 October 2026.
  • The phase 2 trial (220 outpatients, 12 weeks) did not show a significant MADRS reduction versus placebo at 40 mg (pooled mean difference -1.8, p=0.22) or 80 mg (-1.4, p=0.34).
  • At 40 mg, secondary patient-rated scales favored NSI-189 (Symptoms of Depression Questionnaire, p=0.04; Cognitive and Physical Functioning Questionnaire, p=0.03).
  • The phase 1B study (24 inpatients, 6 per active arm) reported no serious adverse effects and a half-life of 17.4 to 20.5 hours.
  • Neurogenesis and cognition results come from cells and rodents, and the stroke, irradiation, diabetes and Angelman syndrome studies had developer co-authors.
  • A PubMed search on 9 October 2026 for NSI-189 with trenbolone returned 0 records; the six records for broader terms involved no anabolic steroid.

What is NSI-189 phosphate, and is it approved?

NSI-189 phosphate is an investigational compound with no FDA approval record. openFDA queries for NSI-189 and for amdiglurax returned no application on 9 October 2026.

NSI-189 phosphate is the 1:1 phosphate salt of NSI-189 (PubChem CID 50922680, C22H33N4O5P, 464.5 g/mol, CAS 1270138-41-4). The free base is a separate record (CID 50922681, C22H30N4O, 366.5 g/mol, CAS 1270138-40-3). PubChem lists amdiglurax as a name for the free base and amdiglurax phosphate for the salt.

The human trials tested NSI-189 phosphate. Their abstracts do not say whether doses are expressed as salt or base, so milligram amounts should not be converted between the two.

openFDA Drugs@FDA queries for NSI-189 and for amdiglurax returned no application on 9 October 2026. That is a dated, US-scoped search, and approvals outside the United States are not covered here.

ClinicalTrials.gov also lists trials of a compound coded ALTO-100 in major depressive disorder. Registry searches for NSI-189 and for amdiglurax do not return them, and no record reviewed links that code to NSI-189, so nothing from those trials is attributed to NSI-189 on this page.

PubChem: NSI-189 free base and phosphate salt identity

Chemical identity record

National Library of Medicine. PubChem compound records CID 50922681 (NSI-189) and CID 50922680 (NSI-189 phosphate, 1:1 salt).

Free base NSI-189: CID 50922681, C22H30N4O, 366.5 g/mol, CAS 1270138-40-3. NSI-189 phosphate (1:1 salt): CID 50922680, C22H33N4O5P, 464.5 g/mol, CAS 1270138-41-4. PubChem lists amdiglurax as a name for the free base and amdiglurax phosphate for the salt. The human trials tested NSI-189 phosphate, and their abstracts do not say whether doses are expressed as salt or base.

Participants / model
Chemical identity, not a clinical population
Treatment
Free base and phosphate salt
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. Milligram amounts should not be converted between salt and base.

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 queries run on 9 October 2026 for NSI-189 and for amdiglurax by brand or generic name.

The queries for NSI-189 and for amdiglurax returned no application. No US approval record was found. This supports only a dated, US-scoped statement.

Participants / model
FDA application database, not a clinical population
Treatment
Name searches
Follow-up
Queries 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 depression trials find?

The phase 2 trial in 220 outpatients with major depressive disorder missed its primary endpoint at both doses. At 40 mg, secondary patient-rated scales favored NSI-189, and the phase 1B study reported no serious adverse effects.

The phase 2 trial randomized 220 adult outpatients with major depressive disorder to oral NSI-189 phosphate 40 mg daily, 80 mg daily or placebo for 12 weeks as monotherapy, using a sequential parallel comparison design. The primary measure was the MADRS. The reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34).

On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03) and the QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated, and Neuralstem employees were among the authors.

The phase 1B study randomized 24 inpatients with major depressive disorder in three cohorts to NSI-189 phosphate 40 mg once, twice or three times daily (6 per cohort) or placebo (2 per cohort) for 28 days, with outpatient follow-up to day 84. Exploratory measures (the Symptoms of Depression Questionnaire, MADRS, CGI-I and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up. The authors name the small cohorts as the main limitation. With 6 people per active arm, this is a tolerability study with exploratory efficacy.

Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source
Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source

What did the post hoc analysis of the phase 2 trial add?

Splitting the phase 2 patients at a baseline MADRS of 30, the 80 mg dose separated from placebo only in the moderately depressed subgroup. Post hoc subgroup results do not change the primary result.

A post hoc analysis of the phase 2 trial split patients at a baseline MADRS of 30. In the moderately depressed subgroup (MADRS below 30), 80 mg separated from placebo on the six-item MADRS (P=.046). It did not in the severely depressed subgroup. CogScreen variables improved in 11 of 36 patients (31%) in the moderate subgroup, 5 of 36 (14%) in the severe subgroup and 7 of 36 (19%) in the whole group.

Post hoc subgroup results do not change the primary result of the phase 2 trial. The abstract's conclusion calls NSI-189 an effective and safe adjunctive therapy, although the phase 2 report describes the trial as monotherapy.

Post hoc analysis: phase 2 split at baseline MADRS 30

Clinical trial

Johe KK et al. Ann Clin Psychiatry. 2020;32(3):182-196. PMID 32722729.

In the moderately depressed subgroup (MADRS below 30), 80 mg separated from placebo on the six-item MADRS (P=.046); it did not in the severely depressed subgroup. CogScreen variables improved in 11 of 36 (31%) in the moderate subgroup, 5 of 36 (14%) in the severe subgroup, and 7 of 36 (19%) in the whole group.

Participants / model
Subgroups of the 220 phase 2 outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily
Follow-up
12 weeks
Study design
Post hoc analysis of a randomized trial
Funding
not stated in the source

Post hoc subgroup results do not change the primary result of the phase 2 trial. The abstract's conclusion calls NSI-189 an effective and safe adjunctive therapy, although the phase 2 report describes the trial as monotherapy.

Read the original source
Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source

Which NSI-189 studies are registered, and what has been published?

The phase 2 trial is registered with status unknown and no posted results, so its published report is the only source of its outcome. Three other registered NSI-189 studies also have no posted results.

ClinicalTrials.gov lists the phase 2 trial (NCT02695472, enrollment 220) with status unknown and no posted results. The published report is the only source of its outcome.

The registry also lists a completed single-dose PK study (NCT01310881, enrollment 35), a completed multiple-dose PK and pharmacodynamic study in patients with depression (NCT01520649, enrollment 26), and a longitudinal observational cohort study in outpatients with major depressive disorder (NCT02724735, enrollment 220, status unknown). None has posted results.

An erratum to the phase 1B paper has been published (PMID 27528461). Its content is not described here.

Registry: phase 2 status unknown, no posted results

Trial registry record

ClinicalTrials.gov. NCT02695472 (phase 2), with related records NCT01310881, NCT01520649 and NCT02724735.

The phase 2 trial (NCT02695472, enrollment 220) is listed with status unknown and no posted results; the published report is the only source of its outcome. The registry also lists a completed single-dose PK study (NCT01310881, enrollment 35), a completed multiple-dose PK and pharmacodynamic study in patients with depression (NCT01520649, enrollment 26), and a longitudinal observational cohort study in outpatients with major depressive disorder (NCT02724735, enrollment 220, status unknown), none with posted results.

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

No posted results for any of the four records.

Read the original source
Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source

What do the cell and rodent studies show?

In cells and rodents, NSI-189 increased neurogenesis markers and improved cognitive or motor measures in stroke, irradiation, diabetes and Angelman syndrome models. These studies had developer co-authors, and none is a human result.

The compound entered depression trials on preclinical data showing stimulation of neurogenesis in human hippocampus-derived neural stem cells in vitro and in mouse hippocampus in vivo. In Angelman syndrome model mice and wild-type mice, NSI-189 increased theta-burst long-term potentiation in hippocampal slices, and a short course of daily injections reversed cognitive and motor impairments in the model mice while slightly improving wild-type performance. The effects were associated with activation of the TrkB and Akt pathways.

In adult Sprague-Dawley rats after middle cerebral artery occlusion, oral NSI-189 started 6 hours after stroke and given daily for 12 weeks reduced motor and neurological deficits, with benefit maintained to 24 weeks, and increased neurite outgrowth (MAP2) mainly in the hippocampus. In vitro, it reduced hippocampal cell death after oxygen-glucose deprivation and raised BDNF and SCF.

In Long-Evans rats given fractionated cranial irradiation, four weeks of daily oral NSI-189 improved performance on all four spontaneous exploration tasks (novel place recognition, novel object recognition, object in place, temporal order), with a trend on contextual fear conditioning, and the benefit persisted one month after treatment stopped. Treated rats had more neurogenesis and fewer activated microglia than irradiated controls, without major change in hippocampal volume.

In mouse models of type 1 diabetes (female) and type 2 diabetes (male), oral NSI-189 prevented multiple functional and anatomical indices of peripheral neuropathy, increased hippocampal neurogenesis, synaptic markers and volume, protected long-term memory, and halted progression of established neuropathy. In cultured adult rat sensory neurons it enhanced neurite outgrowth and mitochondrial function.

The results are consistent across these models. The Angelman, stroke, irradiation and diabetes studies each had developer co-authors, and the abstracts do not give the doses.

Mice: long-term potentiation and TrkB and Akt activation

Animal study

Liu Y et al. Neuropharmacology. 2019;144:337-344. PMID 30408487.

The compound was taken into depression trials on preclinical data showing stimulation of neurogenesis in human hippocampus-derived neural stem cells in vitro and in mouse hippocampus in vivo. In this study, NSI-189 increased theta-burst long-term potentiation in hippocampal slices from wild-type and Angelman syndrome model mice, and a short course of daily injections reversed cognitive and motor impairments in the model mice while slightly improving wild-type performance. The effects were associated with activation of the TrkB and Akt pathways.

Participants / model
Hippocampal slices; Angelman syndrome model mice and wild-type mice
Treatment
Slice incubation; daily injections (route not stated in the abstract)
Follow-up
Short course of daily injections
Study design
Preclinical study of long-term potentiation, cognitive and motor tests, and TrkB and Akt signaling
Funding
not stated in the source

Developer co-authors. The abstract does not give the injection route or dose.

Read the original source
Rats after stroke: oral, 12 weeks, benefit to 24 weeks

Animal study

Tajiri N et al. J Cell Physiol. 2017;232(10):2731-2740. PMID 28181668.

Oral NSI-189 started 6 hours after stroke and given daily for 12 weeks reduced motor and neurological deficits, with benefit maintained to 24 weeks, and increased neurite outgrowth (MAP2) mainly in the hippocampus. In vitro, it reduced hippocampal cell death after oxygen-glucose deprivation and raised BDNF and SCF.

Participants / model
Adult Sprague-Dawley rats with experimental ischemic stroke; hippocampal cells in vitro
Treatment
Oral NSI-189 daily, started 6 hours after middle cerebral artery occlusion
Follow-up
12 weeks of treatment, with benefit followed to 24 weeks
Study design
Preclinical stroke model with motor and neurological scores, MAP2 histology and cell-death assays
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose.

Read the original source
Rats after cranial irradiation: 4 weeks, benefit persisted one month

Animal study

Allen BD et al. Radiat Res. 2018;189(4):345-353. PMID 29351056.

Four weeks of daily oral NSI-189 improved performance on all four spontaneous exploration tasks (novel place recognition, novel object recognition, object in place, temporal order), with a trend on contextual fear conditioning, and the benefit persisted one month after treatment stopped. Treated rats had more neurogenesis and fewer activated microglia than irradiated controls, without major change in hippocampal volume.

Participants / model
Long-Evans rats after fractionated cranial irradiation
Treatment
Oral gavage, daily
Follow-up
4 weeks of treatment, with testing one month after it stopped
Study design
Preclinical study of cognitive tasks, neurogenesis, microglial activation and hippocampal volume
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose.

Read the original source
Diabetic mice: neuropathy, hippocampal neurogenesis and memory

Animal study

Jolivalt CG et al. Diabetes. 2019;68(11):2143-2154. PMID 31492662.

In mouse models of type 1 diabetes (female) and type 2 diabetes (male), oral NSI-189 prevented multiple functional and anatomical indices of peripheral neuropathy, increased hippocampal neurogenesis, synaptic markers, and volume, protected long-term memory, and halted progression of established neuropathy. In cultured adult rat sensory neurons it enhanced neurite outgrowth and mitochondrial function.

Participants / model
Female type 1 and male type 2 diabetic mouse models; cultured adult rat sensory neurons
Treatment
Oral NSI-189
Follow-up
not stated in the source
Study design
Preclinical study of peripheral nerve function and structure, hippocampal neurogenesis and volume, and memory
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose or duration.

Read the original source

Does NSI-189 help recovery from trenbolone, and were the phase 2 data promising?

No study tests recovery from trenbolone in any species: a PubMed search on 9 October 2026 for NSI-189 with trenbolone returned 0 records. Calling the phase 2 data promising leaves out that the primary endpoint was missed.

Sellers describe NSI-189 as helping depression, cognition, memory and neuroregeneration, as having a role in recovery from compounds such as trenbolone, and as having promising phase 2 depression data.

A PubMed search on 9 October 2026 for NSI-189, NSI189 or "NSI 189" with trenbolone returned 0 records. Broadening to trenbolone, anabolic, androgen or steroid returned 6 records: the phase 1B trial, a 2017 review, the rat stroke study, a 2022 rat diabetes study, the mouse alprazolam study, and a serum metabolomics study in pregnant women with thyroid autoimmunity that lists NSI-189 among its metabolite features. None involves trenbolone or any anabolic steroid. A ClinicalTrials.gov search for NSI-189 with trenbolone returned no studies.

The nearest drug-induced deficit model is not an anabolic steroid. In mice given alprazolam repeatedly for 24 days, memory consolidation declined, and co-administration of NSI-189 rescued it. That is co-treatment during exposure to a benzodiazepine, not recovery after stopping a drug.

On the phase 2 data, the primary endpoint was missed at both doses. The cognition signal is secondary and partly post hoc, and neuroregeneration is shown only in rodents and cells.

PubMed search, 9 October 2026: 0 records with trenbolone, 6 with the broader terms

PubMed search record

PubMed search run on 9 October 2026: (NSI-189 OR NSI189 OR "NSI 189") AND (trenbolone OR anabolic OR androgen OR steroid). 6 records returned; the same names with trenbolone alone returned 0 records.

A search for NSI-189, NSI189 or "NSI 189" with trenbolone returned 0 records. Broadening to trenbolone, anabolic, androgen or steroid returned 6 records: the phase 1B trial, a 2017 review, the rat stroke study, a 2022 rat diabetes study, the mouse alprazolam study, and a serum metabolomics study in pregnant women with thyroid autoimmunity that lists NSI-189 among its metabolite features. None involves trenbolone or any anabolic steroid. A ClinicalTrials.gov search for NSI-189 with trenbolone returned no studies. Recovery from trenbolone has no study in any species among these records.

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

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

Read the original source
Mice on repeated alprazolam: memory rescued by co-treatment

Animal study

Zhu S et al. Aging (Albany NY). 2023;15(19):10428-10452. PMID 37801512.

In mice given alprazolam repeatedly for 24 days, memory consolidation declined, and co-administration of NSI-189 rescued it.

Participants / model
Mice given repeated alprazolam
Treatment
NSI-189 co-administered with alprazolam (route and dose not stated in the abstract)
Follow-up
24 days of alprazolam
Study design
Preclinical study of memory consolidation (IntelliCage, novel object recognition), hippocampal histology and BDNF
Funding
not stated in the source

This is co-treatment during exposure to a benzodiazepine in mice. It is not recovery after stopping a drug, and not an anabolic steroid.

Read the original source
Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source
Post hoc analysis: phase 2 split at baseline MADRS 30

Clinical trial

Johe KK et al. Ann Clin Psychiatry. 2020;32(3):182-196. PMID 32722729.

In the moderately depressed subgroup (MADRS below 30), 80 mg separated from placebo on the six-item MADRS (P=.046); it did not in the severely depressed subgroup. CogScreen variables improved in 11 of 36 (31%) in the moderate subgroup, 5 of 36 (14%) in the severe subgroup, and 7 of 36 (19%) in the whole group.

Participants / model
Subgroups of the 220 phase 2 outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily
Follow-up
12 weeks
Study design
Post hoc analysis of a randomized trial
Funding
not stated in the source

Post hoc subgroup results do not change the primary result of the phase 2 trial. The abstract's conclusion calls NSI-189 an effective and safe adjunctive therapy, although the phase 2 report describes the trial as monotherapy.

Read the original source

How does NSI-189 work, and what does the body do with it?

Cell and rodent studies link NSI-189 to neurogenesis and to TrkB and Akt activation, and none of the human trial endpoints in these sources measured neurogenesis. In the phase 1B study, half-life was 17.4 to 20.5 hours.

The mechanisms described come from cells and rodents. NSI-189 stimulated neurogenesis in human hippocampus-derived neural stem cells in vitro and in mouse hippocampus in vivo. In mice, it increased theta-burst long-term potentiation, and its effects were associated with activation of the TrkB and Akt pathways. In rats, it raised BDNF and SCF in vitro and increased neurite outgrowth after stroke.

The human trial endpoints in these sources were symptom scales, cognitive tests, safety and PK. None measured neurogenesis, so the cell and rodent mechanism is not shown in people.

In the phase 1B study in 24 inpatients with major depressive disorder, AUC rose in a dose-related, nearly proportional way and half-life was 17.4 to 20.5 hours. The abstract does not state the route.

Mice: long-term potentiation and TrkB and Akt activation

Animal study

Liu Y et al. Neuropharmacology. 2019;144:337-344. PMID 30408487.

The compound was taken into depression trials on preclinical data showing stimulation of neurogenesis in human hippocampus-derived neural stem cells in vitro and in mouse hippocampus in vivo. In this study, NSI-189 increased theta-burst long-term potentiation in hippocampal slices from wild-type and Angelman syndrome model mice, and a short course of daily injections reversed cognitive and motor impairments in the model mice while slightly improving wild-type performance. The effects were associated with activation of the TrkB and Akt pathways.

Participants / model
Hippocampal slices; Angelman syndrome model mice and wild-type mice
Treatment
Slice incubation; daily injections (route not stated in the abstract)
Follow-up
Short course of daily injections
Study design
Preclinical study of long-term potentiation, cognitive and motor tests, and TrkB and Akt signaling
Funding
not stated in the source

Developer co-authors. The abstract does not give the injection route or dose.

Read the original source
Rats after stroke: oral, 12 weeks, benefit to 24 weeks

Animal study

Tajiri N et al. J Cell Physiol. 2017;232(10):2731-2740. PMID 28181668.

Oral NSI-189 started 6 hours after stroke and given daily for 12 weeks reduced motor and neurological deficits, with benefit maintained to 24 weeks, and increased neurite outgrowth (MAP2) mainly in the hippocampus. In vitro, it reduced hippocampal cell death after oxygen-glucose deprivation and raised BDNF and SCF.

Participants / model
Adult Sprague-Dawley rats with experimental ischemic stroke; hippocampal cells in vitro
Treatment
Oral NSI-189 daily, started 6 hours after middle cerebral artery occlusion
Follow-up
12 weeks of treatment, with benefit followed to 24 weeks
Study design
Preclinical stroke model with motor and neurological scores, MAP2 histology and cell-death assays
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose.

Read the original source
Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source

What risks did the studies report?

The phase 1B study reported no serious adverse effects, and the phase 2 report said both doses were well tolerated. These are small, short studies, and the longest dosing was 12 weeks.

The phase 1B study, in 24 inpatients dosed for 28 days, reported NSI-189 as relatively well tolerated with no serious adverse effects. The phase 2 report, in 220 outpatients dosed for 12 weeks, said both doses were well tolerated.

Those are the only human safety statements in the sources reviewed. The phase 1B cohorts had 6 people per active arm, the longest dosing was 12 weeks, and this page gives no adverse-event rates. No safety information is available for the supplier uses, including use alongside anabolic steroids.

Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source
Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source

Why does NSI-189 sit in D tier?

The one adequately sized human trial missed its primary endpoint at both doses, and the positive results were secondary or post hoc. The rodent work is consistent but largely from the developer, and the trenbolone claim has no study behind it.

The phase 2 trial in 220 patients missed its primary endpoint. The positive results were limited to secondary patient-rated scales and some CogScreen measures at 40 mg, concentrated in stage 2 of the design, plus a post hoc subgroup analysis. The phase 1B study had 6 people per active arm.

Rodent results for neurogenesis and cognition are consistent across stroke, irradiation, diabetes, Angelman syndrome and benzodiazepine models, so the mechanism stays plausible. Most of that work had developer co-authors, and the human efficacy test failed.

On the supplier's claims, the phase 2 data cannot fairly be called promising without noting the missed primary endpoint, neuroregeneration is shown only in rodents and cells, and recovery from trenbolone has no study in any species.

Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source
Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source
Post hoc analysis: phase 2 split at baseline MADRS 30

Clinical trial

Johe KK et al. Ann Clin Psychiatry. 2020;32(3):182-196. PMID 32722729.

In the moderately depressed subgroup (MADRS below 30), 80 mg separated from placebo on the six-item MADRS (P=.046); it did not in the severely depressed subgroup. CogScreen variables improved in 11 of 36 (31%) in the moderate subgroup, 5 of 36 (14%) in the severe subgroup, and 7 of 36 (19%) in the whole group.

Participants / model
Subgroups of the 220 phase 2 outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily
Follow-up
12 weeks
Study design
Post hoc analysis of a randomized trial
Funding
not stated in the source

Post hoc subgroup results do not change the primary result of the phase 2 trial. The abstract's conclusion calls NSI-189 an effective and safe adjunctive therapy, although the phase 2 report describes the trial as monotherapy.

Read the original source
PubMed search, 9 October 2026: 0 records with trenbolone, 6 with the broader terms

PubMed search record

PubMed search run on 9 October 2026: (NSI-189 OR NSI189 OR "NSI 189") AND (trenbolone OR anabolic OR androgen OR steroid). 6 records returned; the same names with trenbolone alone returned 0 records.

A search for NSI-189, NSI189 or "NSI 189" with trenbolone returned 0 records. Broadening to trenbolone, anabolic, androgen or steroid returned 6 records: the phase 1B trial, a 2017 review, the rat stroke study, a 2022 rat diabetes study, the mouse alprazolam study, and a serum metabolomics study in pregnant women with thyroid autoimmunity that lists NSI-189 among its metabolite features. None involves trenbolone or any anabolic steroid. A ClinicalTrials.gov search for NSI-189 with trenbolone returned no studies. Recovery from trenbolone has no study in any species among these records.

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

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

Read the original source

Studies and sources

PubChem: NSI-189 free base and phosphate salt identity

Chemical identity record

National Library of Medicine. PubChem compound records CID 50922681 (NSI-189) and CID 50922680 (NSI-189 phosphate, 1:1 salt).

Free base NSI-189: CID 50922681, C22H30N4O, 366.5 g/mol, CAS 1270138-40-3. NSI-189 phosphate (1:1 salt): CID 50922680, C22H33N4O5P, 464.5 g/mol, CAS 1270138-41-4. PubChem lists amdiglurax as a name for the free base and amdiglurax phosphate for the salt. The human trials tested NSI-189 phosphate, and their abstracts do not say whether doses are expressed as salt or base.

Participants / model
Chemical identity, not a clinical population
Treatment
Free base and phosphate salt
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. Milligram amounts should not be converted between salt and base.

Read the original source
Phase 1B: 24 inpatients, 28 days, no serious adverse effects

Randomized controlled trial

Fava M et al. Mol Psychiatry. 2016;21(10):1372-80. PMID 26643541.

NSI-189 was relatively well tolerated with no serious adverse effects. AUC rose in a dose-related, nearly proportional way, and half-life was 17.4 to 20.5 hours. Exploratory measures (Symptoms of Depression Questionnaire, MADRS, CGI-I, and the MGH Cognitive and Physical Functioning Questionnaire) favored NSI-189, with significant improvement on the Symptoms of Depression Questionnaire and the Cognitive and Physical Functioning Questionnaire, and the changes persisted through follow-up.

Participants / model
24 inpatients with major depressive disorder
Treatment
NSI-189 phosphate 40 mg once, twice, or three times daily (6 per cohort) or placebo (2 per cohort); route not stated in the abstract
Follow-up
28 days as inpatients, with outpatient follow-up to day 84
Study design
Randomized trial in three cohorts, with safety, PK and exploratory efficacy measures
Funding
not stated in the source

The authors name the small cohorts as the main limitation. With 6 people per active arm this is a tolerability study with exploratory efficacy. An erratum to this paper exists (PMID 27528461).

Read the original source
Phase 2: 220 outpatients, 12 weeks, primary endpoint missed

Randomized controlled trial

Papakostas GI et al. Mol Psychiatry. 2020;25(7):1569-1579. PMID 30626911.

MADRS reduction versus placebo was not significant at either dose (40 mg pooled mean difference -1.8, p=0.22; 80 mg -1.4, p=0.34). On secondary patient-rated scales, 40 mg beat placebo on the Symptoms of Depression Questionnaire (pooled mean difference -8.2, p=0.04), the Cognitive and Physical Functioning Questionnaire (-1.9, p=0.03), and QIDS-SR in stage 2 only (-2.5, p=0.04). Effect sizes were small in stage 1 and larger in stage 2 (Cohen's d, stage 1 then stage 2: SDQ -0.11 and -0.64; CPFQ -0.28 and -0.47; QIDS-SR -0.03 and -0.68). The 40 mg dose also showed advantages on some CogScreen measures (absolute d 0.12 to 1.12, p values 0.002 to 0.048 for those with overall significance) but not on the Cogstate battery. The abstract reports secondary advantages only for 40 mg. Both doses were well tolerated.

Participants / model
220 adult outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily, or placebo, as monotherapy
Follow-up
12 weeks
Study design
Randomized placebo-controlled trial, sequential parallel comparison design
Funding
not stated in the source

The primary endpoint (MADRS) was missed at both doses. Neuralstem employees were among the authors. Secondary endpoints were SDQ, CPFQ, QIDS-SR, CogScreen and Cogstate.

Read the original source
Post hoc analysis: phase 2 split at baseline MADRS 30

Clinical trial

Johe KK et al. Ann Clin Psychiatry. 2020;32(3):182-196. PMID 32722729.

In the moderately depressed subgroup (MADRS below 30), 80 mg separated from placebo on the six-item MADRS (P=.046); it did not in the severely depressed subgroup. CogScreen variables improved in 11 of 36 (31%) in the moderate subgroup, 5 of 36 (14%) in the severe subgroup, and 7 of 36 (19%) in the whole group.

Participants / model
Subgroups of the 220 phase 2 outpatients with major depressive disorder
Treatment
Oral NSI-189 phosphate 40 or 80 mg daily
Follow-up
12 weeks
Study design
Post hoc analysis of a randomized trial
Funding
not stated in the source

Post hoc subgroup results do not change the primary result of the phase 2 trial. The abstract's conclusion calls NSI-189 an effective and safe adjunctive therapy, although the phase 2 report describes the trial as monotherapy.

Read the original source
Registry: phase 2 status unknown, no posted results

Trial registry record

ClinicalTrials.gov. NCT02695472 (phase 2), with related records NCT01310881, NCT01520649 and NCT02724735.

The phase 2 trial (NCT02695472, enrollment 220) is listed with status unknown and no posted results; the published report is the only source of its outcome. The registry also lists a completed single-dose PK study (NCT01310881, enrollment 35), a completed multiple-dose PK and pharmacodynamic study in patients with depression (NCT01520649, enrollment 26), and a longitudinal observational cohort study in outpatients with major depressive disorder (NCT02724735, enrollment 220, status unknown), none with posted results.

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

No posted results for any of the four records.

Read the original source
Mice: long-term potentiation and TrkB and Akt activation

Animal study

Liu Y et al. Neuropharmacology. 2019;144:337-344. PMID 30408487.

The compound was taken into depression trials on preclinical data showing stimulation of neurogenesis in human hippocampus-derived neural stem cells in vitro and in mouse hippocampus in vivo. In this study, NSI-189 increased theta-burst long-term potentiation in hippocampal slices from wild-type and Angelman syndrome model mice, and a short course of daily injections reversed cognitive and motor impairments in the model mice while slightly improving wild-type performance. The effects were associated with activation of the TrkB and Akt pathways.

Participants / model
Hippocampal slices; Angelman syndrome model mice and wild-type mice
Treatment
Slice incubation; daily injections (route not stated in the abstract)
Follow-up
Short course of daily injections
Study design
Preclinical study of long-term potentiation, cognitive and motor tests, and TrkB and Akt signaling
Funding
not stated in the source

Developer co-authors. The abstract does not give the injection route or dose.

Read the original source
Rats after stroke: oral, 12 weeks, benefit to 24 weeks

Animal study

Tajiri N et al. J Cell Physiol. 2017;232(10):2731-2740. PMID 28181668.

Oral NSI-189 started 6 hours after stroke and given daily for 12 weeks reduced motor and neurological deficits, with benefit maintained to 24 weeks, and increased neurite outgrowth (MAP2) mainly in the hippocampus. In vitro, it reduced hippocampal cell death after oxygen-glucose deprivation and raised BDNF and SCF.

Participants / model
Adult Sprague-Dawley rats with experimental ischemic stroke; hippocampal cells in vitro
Treatment
Oral NSI-189 daily, started 6 hours after middle cerebral artery occlusion
Follow-up
12 weeks of treatment, with benefit followed to 24 weeks
Study design
Preclinical stroke model with motor and neurological scores, MAP2 histology and cell-death assays
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose.

Read the original source
Rats after cranial irradiation: 4 weeks, benefit persisted one month

Animal study

Allen BD et al. Radiat Res. 2018;189(4):345-353. PMID 29351056.

Four weeks of daily oral NSI-189 improved performance on all four spontaneous exploration tasks (novel place recognition, novel object recognition, object in place, temporal order), with a trend on contextual fear conditioning, and the benefit persisted one month after treatment stopped. Treated rats had more neurogenesis and fewer activated microglia than irradiated controls, without major change in hippocampal volume.

Participants / model
Long-Evans rats after fractionated cranial irradiation
Treatment
Oral gavage, daily
Follow-up
4 weeks of treatment, with testing one month after it stopped
Study design
Preclinical study of cognitive tasks, neurogenesis, microglial activation and hippocampal volume
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose.

Read the original source
Diabetic mice: neuropathy, hippocampal neurogenesis and memory

Animal study

Jolivalt CG et al. Diabetes. 2019;68(11):2143-2154. PMID 31492662.

In mouse models of type 1 diabetes (female) and type 2 diabetes (male), oral NSI-189 prevented multiple functional and anatomical indices of peripheral neuropathy, increased hippocampal neurogenesis, synaptic markers, and volume, protected long-term memory, and halted progression of established neuropathy. In cultured adult rat sensory neurons it enhanced neurite outgrowth and mitochondrial function.

Participants / model
Female type 1 and male type 2 diabetic mouse models; cultured adult rat sensory neurons
Treatment
Oral NSI-189
Follow-up
not stated in the source
Study design
Preclinical study of peripheral nerve function and structure, hippocampal neurogenesis and volume, and memory
Funding
not stated in the source

Developer co-authors. The abstract does not give the dose or duration.

Read the original source
Mice on repeated alprazolam: memory rescued by co-treatment

Animal study

Zhu S et al. Aging (Albany NY). 2023;15(19):10428-10452. PMID 37801512.

In mice given alprazolam repeatedly for 24 days, memory consolidation declined, and co-administration of NSI-189 rescued it.

Participants / model
Mice given repeated alprazolam
Treatment
NSI-189 co-administered with alprazolam (route and dose not stated in the abstract)
Follow-up
24 days of alprazolam
Study design
Preclinical study of memory consolidation (IntelliCage, novel object recognition), hippocampal histology and BDNF
Funding
not stated in the source

This is co-treatment during exposure to a benzodiazepine in mice. It is not recovery after stopping a drug, and not an anabolic steroid.

Read the original source

Why is NSI-189 phosphate in D tier?

D fits a compound whose one adequately sized human efficacy trial missed its primary endpoint at both doses. The secondary results at 40 mg and a post hoc subgroup do not replace that, the first study in patients had 6 people per active arm, and the neuroregeneration claim rests on cells and rodents, most of it with developer co-authors. The trenbolone recovery use has no study in any species.