TND1128

updated

TND1128 is a 5-deazaflavin derivative that its authors describe as a mitochondria-stimulating, NAD+-assisting substance. The published work is three papers from 2021 to 2024 by one author network with a company link, in cultured mouse neurons and in brain slices from dosed mice. No controlled human study exists, and no ATP measurement, whole-animal functional outcome, pharmacokinetics or toxicology has been published.

5-deazaflavin derivative (described as a mitochondrial activator)

  • PubChem returned no record under the code TND1128 on 10 October 2026; the 2021 paper's chemical name resolves to CID 322148, C14H13N3O2, molecular weight 255.27.
  • In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses; the abstract gives no concentration and no measure of mitochondrial function or ATP.
  • In brain slices from mice pretreated by subcutaneous injection, TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently, while beta-NMN did not significantly affect mitochondrial Ca2+.
  • In slices from mice pretreated by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested; the abstract reports no direct ATP measurement.
  • The three papers share authors, the 2021 abstract lists a company affiliation, and the 2023 paper was funded partially by Chemiteras Corporation; no independent replication exists in the records reviewed.
  • No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity or any whole-animal functional outcome such as cognition or exercise.

What is TND1128, and what is its regulatory status?

TND1128 is a 5-deazaflavin derivative described in three papers from 2021 to 2024. PubChem has no record under the code, and the match to CID 322148 rests on the 2021 paper's chemical name. No label or registered study exists.

PubChem returned no record under the code TND1128 on 10 October 2026. The 2021 paper names the compound 10-ethyl-3-methylpyrimido[4,5-b]quinoline-2,4(3H,10H)-dione, and that name resolves to PubChem CID 322148, C14H13N3O2, molecular weight 255.27, CAS 59997-14-7, with the synonym 3-Methyl-10-ethyl-Deazaflavin. The match between the code and the CID rests on the 2021 paper's own naming, not on a PubChem record for the code. PubChem also lists NSC 278160 as a synonym, and no result for it was reviewed.

A 2023 abstract calls TND1128 a derivative of 5-deazaflavin with efficient self-redox ability, and the 2021 abstract calls it an NAD+-assisting substance.

ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label. Status outside the United States is not covered here.

PubChem: chemical name from the 2021 paper resolves to CID 322148

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 322148, matched to TND1128 through the chemical name given in the 2021 paper.

PubChem returned no record under the code TND1128 on 10 October 2026. The 2021 paper names the compound 10-ethyl-3-methylpyrimido[4,5-b]quinoline-2,4(3H,10H)-dione, and that name resolves to PubChem CID 322148, C14H13N3O2, 255.27 g/mol, CAS 59997-14-7, with the synonym 3-Methyl-10-ethyl-Deazaflavin. A 2023 abstract calls TND1128 a derivative of 5-deazaflavin with efficient self-redox ability, and the 2021 abstract calls it an NAD+-assisting substance.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record, matched through a journal article
Funding
not stated in the source

The match between the code and the CID rests on the 2021 paper's own naming, not on a PubChem record for the code. PubChem lists NSC 278160 as a synonym; no result for it was reviewed.

Read the original source
PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

What did the neuron culture and mouse brain slice studies find?

In cultured mouse neurons, TND1128 induced branching and increased excitatory synapses. In brain slices from pretreated mice, it mitigated calcium dynamics dose-dependently and raised mitochondrial membrane potential. No controlled human study exists, and no ATP measurement or whole-animal outcome has been published.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

In a 2023 paper, brain slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

In a 2024 paper, slices from mice pretreated with TND1128 by intraperitoneal injection showed a significant rise in mitochondrial membrane potential after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement.

2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source

How does TND1128 act on mitochondria?

TND1128 is described as a 5-deazaflavin derivative with efficient self-redox ability. The measured results are membrane potential and calcium changes in slices, and the idea that it enters the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

A 2023 abstract calls TND1128 a derivative of 5-deazaflavin with efficient self-redox ability, and the 2021 abstract calls it an NAD+-assisting substance. These are the authors' descriptions of the chemistry.

What was measured is narrower. In slices from dosed mice, TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently, and mitochondrial membrane potential rose after 24-hour pretreatment at the highest dose tested. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result, and no direct ATP measurement is reported.

PubChem: chemical name from the 2021 paper resolves to CID 322148

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 322148, matched to TND1128 through the chemical name given in the 2021 paper.

PubChem returned no record under the code TND1128 on 10 October 2026. The 2021 paper names the compound 10-ethyl-3-methylpyrimido[4,5-b]quinoline-2,4(3H,10H)-dione, and that name resolves to PubChem CID 322148, C14H13N3O2, 255.27 g/mol, CAS 59997-14-7, with the synonym 3-Methyl-10-ethyl-Deazaflavin. A 2023 abstract calls TND1128 a derivative of 5-deazaflavin with efficient self-redox ability, and the 2021 abstract calls it an NAD+-assisting substance.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record, matched through a journal article
Funding
not stated in the source

The match between the code and the CID rests on the 2021 paper's own naming, not on a PubChem record for the code. PubChem lists NSC 278160 as a synonym; no result for it was reviewed.

Read the original source
2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source

How independent are the three TND1128 papers?

Not independent. Authors Akaike N and Nagamatsu T appear on all three, the 2023 and 2024 papers share first and last authors, and a company is linked to the 2021 and 2023 work. No independent replication exists in the records reviewed.

Akaike N and Nagamatsu T appear on all three papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y. Affiliations on the 2021 abstract include a company, Chemiteras, Inc., Yokohama. The 2023 paper states it was funded partially by Chemiteras Corporation, Kanagawa, with the sponsor having no control over interpretation, writing or publication. The 2021 record's conflict-of-interest statement reports no competing interests.

This fits a description of a small number of Japanese groups, and it also means there is no independent replication in the records reviewed.

2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source

Has TND1128 been tested in people?

No. A PubMed search on 10 October 2026 for TND1128 returned 3 records, and no abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity or any whole-animal functional outcome such as cognition or exercise.

A PubMed search on 10 October 2026 for TND1128 returned 3 records. A broader name query returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128.

No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries returned no studies, and DailyMed returned no label.

PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Is TND1128 a mitochondrial activator from a few Japanese labs?

As a description of the literature, yes. But mitochondrial activator is the authors' label for ex vivo membrane potential and calcium results, not demonstrated ATP output or function in animals or people.

Sellers describe TND1128 as a 5-deazaflavin mitochondrial activator that comes from a few Japanese labs. That is an accurate description of the literature: three papers from 2021 to 2024 by one author network.

The label mitochondrial activator comes from the authors. It summarizes dose-dependent effects on membrane potential and Ca2+ in slices from dosed mice and on neuron morphology in culture. No study measured ATP directly, and none reports a whole-animal functional outcome or any human result.

2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source
PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

What is known about the safety of TND1128?

No human safety, pharmacokinetic or toxicology data exist for TND1128 in the records reviewed, and nothing in them shows harm. The evidence is too thin to describe its safety either way.

No abstract reports TND1128 given to a person, so no human adverse event, tolerability or interaction information exists. No abstract reports its pharmacokinetics or toxicity, and no whole-animal outcome of any kind has been published.

Nothing in the records reviewed shows harm. That is an absence of data and not a finding of safety: the three papers are mouse slice and cell work from one author network, and the dosing in them is not reproduced here.

PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source

Why does TND1128 sit in C tier?

TND1128 sits at the thin end of C: plausible self-redox chemistry and dose-dependent slice and neuron results with no harm shown, but only three papers from one author network with a company link, no ATP measurement, no whole-animal outcome, no pharmacokinetics or toxicology and no human data.

The self-redox chemistry is plausible, and the three papers report dose-dependent effects on membrane potential and Ca2+ in slices from dosed mice and on neuron morphology in culture. Nothing in the records reviewed shows harm.

The data are thin: three papers from 2021 to 2024, one author network with a company link, no independent replication, no ATP measurement, no whole-animal functional outcome, no pharmacokinetics or toxicology, and no human data.

2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source
PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Studies and sources

PubChem: chemical name from the 2021 paper resolves to CID 322148

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 322148, matched to TND1128 through the chemical name given in the 2021 paper.

PubChem returned no record under the code TND1128 on 10 October 2026. The 2021 paper names the compound 10-ethyl-3-methylpyrimido[4,5-b]quinoline-2,4(3H,10H)-dione, and that name resolves to PubChem CID 322148, C14H13N3O2, 255.27 g/mol, CAS 59997-14-7, with the synonym 3-Methyl-10-ethyl-Deazaflavin. A 2023 abstract calls TND1128 a derivative of 5-deazaflavin with efficient self-redox ability, and the 2021 abstract calls it an NAD+-assisting substance.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record, matched through a journal article
Funding
not stated in the source

The match between the code and the CID rests on the 2021 paper's own naming, not on a PubChem record for the code. PubChem lists NSC 278160 as a synonym; no result for it was reviewed.

Read the original source
2021: branching and excitatory synapses in cultured mouse neurons

Cell study

Katsurabayashi S et al. Biochem Biophys Res Commun. 2021;560:146-151. PMID 33989906.

In cultured mouse hippocampal neurons, TND1128 induced branching of axons and dendrites and increased the number of excitatory synapses, and its effect was compared with beta-nicotinamide mononucleotide (beta-NMN). The authors present it as a mitochondria-stimulating drug for improving brain function. The abstract gives no concentration and no measure of mitochondrial function or ATP.

Participants / model
Cultured mouse hippocampal neurons
Treatment
TND1128 in cell culture, compared with beta-NMN; concentration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study, cell culture
Funding
The record's conflict-of-interest statement reports no competing interests; affiliations on the abstract include a company, Chemiteras, Inc., Yokohama

Cultured neurons only. Authors Akaike N and Nagamatsu T appear on all three TND1128 papers.

Read the original source
2023: brain slices after subcutaneous dosing in mice, calcium dynamics

Animal study

Takahashi N et al. J Pharmacol Sci. 2023;151(2):93-109. PMID 36707184.

Slices were prepared from mice 22 +/- 2 hours after pretreatment with TND1128 or beta-NMN, each given by subcutaneous injection at three doses. TND1128 mitigated cytoplasmic and mitochondrial Ca2+ dynamics dose-dependently during repeated high-potassium exposure, while beta-NMN affected cytoplasmic Ca2+ significantly but its effect on mitochondrial Ca2+ was insignificant. The authors conclude TND1128 showed mitochondria-activating potential in this preparation. The mice are described only as mice, and no disease model is named in the abstract.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; species, strain and disease model not stated in the abstract
Treatment
TND1128 or beta-NMN by subcutaneous injection, three doses of each; doses not reproduced here
Follow-up
Slices prepared 22 +/- 2 hours after pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
Funded partially by Chemiteras Corporation, Kanagawa; the paper states the sponsor had no control over interpretation, writing or publication

Authors Akaike N and Nagamatsu T appear on this paper and on the 2021 and 2024 papers, and the 2023 and 2024 papers share first author Takahashi N and last author Kudo Y.

Read the original source
2024: membrane potential rose after 24-hour pretreatment; no direct ATP measurement

Animal study

Takahashi N et al. J Pharmacol Sci. 2024;156(4):218-229. PMID 39608846.

In slices from mice pretreated with TND1128 by intraperitoneal injection, mitochondrial membrane potential rose significantly after 24-hour pretreatment at the highest dose tested, and potassium-induced depolarization and the cytoplasmic and mitochondrial Ca2+ rises were significantly lower in the pretreated preparations. The abstract defines its ATP synthesis index as the inverse of the membrane potential value, so it reports no direct ATP measurement. The statement that TND1128 could be incorporated into the TCA cycle and electron transfer chains is the authors' suggestion, not a measured result.

Participants / model
Mice, with slices prepared ex vivo after in vivo dosing; strain not stated in the abstract
Treatment
TND1128 by intraperitoneal injection across a dose range; doses not reproduced here
Follow-up
24-hour pretreatment
Study design
Original preclinical study, ex vivo slices after in vivo dosing
Funding
not stated in the source

Mitochondrial membrane potential was measured with JC-1, and the ATP synthesis index is derived from it. Authors overlap with the 2021 and 2023 papers.

Read the original source
PubMed: 3 records; no human data; no registered study; no label

PubMed search record

PubMed searches for TND1128, for TND-1128 or TND 1128 or the chemical name, for Akaike N with deazaflavin terms, and for 5-deazaflavin with mitochondria terms, run 10 October 2026, with ClinicalTrials.gov and DailyMed queries.

A PubMed search on 10 October 2026 for TND1128 returned 3 records (PMIDs 33989906, 36707184 and 39608846). A broader name query for TND-1128, TND 1128 or the chemical name returned 1 of the same, Akaike N with deazaflavin terms returned 2 of the same, and 5-deazaflavin with mitochondria terms returned 3, the two J Pharmacol Sci papers and an unrelated survivin inhibitor paper. Other 5-deazaflavin hits in a wider search concerned bacterial cofactors or other derivatives designed as antitumor agents and were not about TND1128. No abstract reports TND1128 given to a person, or its pharmacokinetics, toxicity, or any functional outcome in a whole animal such as cognition or exercise. ClinicalTrials.gov queries for TND1128, 5-deazaflavin and deazaflavin mitochondria activator returned no studies, and DailyMed returned no label.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature, registry and label search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Why is TND1128 in C tier?

C, at the thin end of the grade, fits a compound with plausible self-redox chemistry, dose-dependent effects in slices from dosed mice and in cultured neurons, and no harm shown in the records reviewed. The data are thin: three papers from one author network with a company link, no independent replication, no ATP measurement, no whole-animal outcome, no pharmacokinetics or toxicology and no human data.