JBSNF-000088

updated

JBSNF-000088 (6-methoxynicotinamide) is a small-molecule nicotinamide analog that inhibits nicotinamide N-methyltransferase (NNMT), sold for fat loss and metabolic improvement. Its metabolic evidence is a single originating mouse paper from industry authors, and no controlled human study exists. The abstract reports body weight, not fat mass, so fat loss is not shown for this compound.

Nicotinamide N-methyltransferase (NNMT) inhibitor, nicotinamide analog

  • JBSNF-000088 is a synonym on PubChem CID 250810, 6-methoxypyridine-3-carboxamide (6-methoxynicotinamide), C7H8N2O2, molecular weight 152.15; JBSNF-000028 is a different tricyclic molecule from the same program.
  • In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity and normalized glucose tolerance to the level of lean control mice, and these effects were not seen in NNMT knockout mice. The abstract gives no dose, route or duration.
  • In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss.
  • The originating 2018 paper reports body weight, not fat mass, and its authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys.
  • A PubMed query on 10 October 2026 for JBSNF returned 6 records, all mouse or cell work or tool use, and a query for NNMT inhibitors with clinical trial filters returned 0 records.
  • Outside groups use it as an NNMT tool in a mouse endometriosis model and in gallbladder carcinoma xenografts, which does not test the fat loss claim.

What is JBSNF-000088, and what is its regulatory status?

JBSNF-000088 is 6-methoxynicotinamide, a small-molecule analog of nicotinamide that inhibits nicotinamide N-methyltransferase (NNMT). DailyMed returned no label and ClinicalTrials.gov no study.

JBSNF-000088 is listed as a synonym on PubChem CID 250810, 6-methoxypyridine-3-carboxamide (6-methoxynicotinamide), C7H8N2O2, molecular weight 152.15, CAS 7150-23-4. The 2018 paper describes it as a small molecule analog of nicotinamide. JBSNF-000028, a related compound from the same program, is a different tricyclic molecule and is not the same material.

DailyMed returned no label for JBSNF-000088 or 6-methoxynicotinamide, and ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies. Status outside the United States is not covered here.

PubChem: 6-methoxynicotinamide, JBSNF-000088 listed as a synonym

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 250810, 6-methoxypyridine-3-carboxamide.

JBSNF-000088 is listed as a synonym on PubChem CID 250810, 6-methoxypyridine-3-carboxamide (6-methoxynicotinamide), C7H8N2O2, 152.15 g/mol, CAS 7150-23-4. The 2018 paper describes it as a small molecule analog of nicotinamide.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined small molecule, no salt form
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. JBSNF-000028, a related compound from the same program, is a different tricyclic molecule and is not the same material.

Read the original source
PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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 mouse studies find?

In mice with high fat diet induced obesity, JBSNF-000088 reduced body weight, improved insulin sensitivity and normalized glucose tolerance to the level of lean control mice. In ob/ob and db/db mice it improved glucose handling less and without weight loss. The abstract reports body weight, not fat mass, and no controlled human study exists.

The originating 2018 paper reports that JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity.

In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss.

The abstract reports body weight, not fat mass, and gives no dose, route or duration. The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys, and this is the only originating metabolic paper, with no independent replication of the metabolic result in the records reviewed.

2018 originating paper: body weight, insulin sensitivity and glucose in obese mice

Animal study

Kannt A et al. Sci Rep. 2018;8(1):3660. PMID 29483571.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

Participants / model
Mice with high fat diet induced obesity; NNMT knockout mice; ob/ob and db/db mice
Treatment
JBSNF-000088; dose, route and duration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (industry authors)
Funding
The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys

The abstract reports body weight, not fat mass. A single originating metabolic paper with industry authors and no independent replication of the metabolic result in the records reviewed.

Read the original source

Has JBSNF-000088 been used in disease models other than obesity?

Yes, by outside groups, in cancer and endometriosis work. It reduced lesion weight and number in a mouse endometriosis model and compromised tumor development in gallbladder carcinoma xenografts. These show it is used as an NNMT tool and do not test the fat loss claim.

In a mouse endometriosis model JBSNF-000088 markedly reduced lesion weight and number, and it attenuated proliferation, migration and invasion of endometrial stromal cells. In xenografted gallbladder carcinoma models overexpressing NNMT it compromised tumor development and altered immune marker expression. The in vivo route is not stated in the abstracts.

It also inhibited proliferation of drug-resistant lung cancer cells (PMID 40679940) and was used in ovarian cancer cell lines (PMID 41511664). In a 2025 comparison of NNMT inhibitors including 6-methoxynicotinamide, treated osteosarcoma and Merkel cell carcinoma cells had significantly reduced viability, increased reactive oxygen species and activated apoptotic pathways (PMID 41301471).

These show the compound is in use by outside groups as an NNMT tool and that it reduces cell viability in several cell types. They do not test or support the supplier's fat loss claim.

Outside group: lesion weight and number reduced in a mouse endometriosis model

Animal study

Hou S et al. Cell Death Discov. 2024;10(1):463. PMID 39489776.

In a mouse endometriosis model JBSNF-000088 markedly reduced lesion weight and number, and it attenuated proliferation, migration and invasion of endometrial stromal cells.

Participants / model
A mouse endometriosis model; endometrial stromal cells
Treatment
JBSNF-000088 in vivo and in cell culture; in vivo route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study by an outside group
Funding
not stated in the source

Shows outside use of the compound as an NNMT tool. Other outside uses without separate links: drug-resistant lung cancer cells (PMID 40679940), ovarian cancer cell lines (PMID 41511664) and a 2025 comparison of NNMT inhibitors including 6-methoxynicotinamide in which treated osteosarcoma and Merkel cell carcinoma cells had significantly reduced viability, increased reactive oxygen species and activated apoptotic pathways (PMID 41301471). None tests the fat loss claim.

Read the original source
Outside group: tumor development compromised in gallbladder carcinoma xenografts

Animal study

Li Y et al. Hepatology. 2023;78(5):1352-1367. PMID 36633260.

In xenografted gallbladder carcinoma models overexpressing NNMT, JBSNF-000088 compromised tumor development and altered immune marker expression.

Participants / model
Xenografted gallbladder carcinoma models overexpressing NNMT
Treatment
JBSNF-000088; route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study by an outside group
Funding
not stated in the source

Shows outside use of the compound as an NNMT tool. It does not test the fat loss claim.

Read the original source

How does JBSNF-000088 act on NNMT?

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide levels. A co-crystal structure showed its N-methylated product bound to NNMT, and the authors suggest it acts as a slow-turnover substrate analog. Its effects were absent in NNMT knockout mice, which the authors take as evidence of specificity.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

The metabolic effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. The sibling compound JBSNF-000028 behaved differently: its glucose tolerance improvement persisted in knockout mice, which the authors say points to an effect that may go beyond NNMT inhibition.

2018 originating paper: body weight, insulin sensitivity and glucose in obese mice

Animal study

Kannt A et al. Sci Rep. 2018;8(1):3660. PMID 29483571.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

Participants / model
Mice with high fat diet induced obesity; NNMT knockout mice; ob/ob and db/db mice
Treatment
JBSNF-000088; dose, route and duration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (industry authors)
Funding
The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys

The abstract reports body weight, not fat mass. A single originating metabolic paper with industry authors and no independent replication of the metabolic result in the records reviewed.

Read the original source
2022 paper on the sibling compound JBSNF-000028: effect persisted in knockout mice

Animal study

Ruf S et al. Sci Rep. 2022;12(1):15440. PMID 36104373.

A 2022 paper from the same program describes JBSNF-000028, a different tricyclic NNMT inhibitor that reduced MNA in mouse plasma, liver and adipose tissue and drove insulin sensitization, glucose modulation and body weight reduction in a diet-induced obese mouse model. It was inactive against a broad panel of targets related to metabolism and safety. Its improvement in glucose tolerance was also seen in NNMT knockout mice with diet-induced obesity, which the authors say points to a glucose-normalizing effect that may go beyond NNMT inhibition.

Participants / model
Diet-induced obese mice, including NNMT knockout mice (JBSNF-000028)
Treatment
JBSNF-000028; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (different compound)
Funding
not stated in the source

These findings are for JBSNF-000028, not JBSNF-000088. For JBSNF-000088 the 2018 paper reports the opposite pattern, with effects absent in knockout mice, so the specificity evidence differs between the two compounds.

Read the original source

Has JBSNF-000088 been tested in people?

No. A PubMed query on 10 October 2026 for NNMT inhibitors with clinical trial filters returned 0 records, a query for JBSNF returned 6 records that were all mouse or cell work or tool use, and ClinicalTrials.gov returned no studies. No pharmacokinetic figures appear in the abstracts reviewed.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries returned no studies, and DailyMed returned no label for either name.

A PubMed query for JBSNF-000088 or 6-methoxynicotinamide with pharmacokinetic, bioavailability, oral or plasma returned 1 record, the 2018 paper, whose abstract reports only that the N-methylated product was detected in plasma of treated mice. It gives no exposure, half-life, bioavailability or dose figures.

PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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
PubMed: 1 record, no exposure, half-life or bioavailability figures

PubMed search record

PubMed search for (JBSNF-000088 OR 6-methoxynicotinamide) AND (pharmacokinetic OR bioavailability OR oral OR plasma), run 10 October 2026.

A PubMed query on 10 October 2026 for JBSNF-000088 or 6-methoxynicotinamide with pharmacokinetic, bioavailability, oral or plasma returned 1 record, the 2018 paper, whose abstract reports only that the N-methylated product was detected in plasma of treated mice. It gives no exposure, half-life, bioavailability or dose figures.

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

An absence finding as of 10 October 2026, based on abstracts. Any pharmacokinetic values would be in the full text, which this page does not summarize.

Read the original source

Does JBSNF-000088 cause fat loss?

Not shown. In diet-induced obese mice it lowered body weight and improved insulin sensitivity and glucose tolerance, but the abstract reports body weight and not fat mass, and it gave glucose benefit without weight loss in two genetic obesity models. Nothing was tested in people.

Sellers market JBSNF-000088 for fat loss and metabolic improvement, on the same target as 5-amino-1MQ. The mouse data support lower body weight, better insulin sensitivity and normalized glucose tolerance in diet-induced obesity, with glucose benefit but no weight loss in two genetic obesity models.

The abstract reports body weight, not fat mass, so this page does not claim fat loss for this compound, even in mice. The result comes from a single originating metabolic paper by industry authors, with no independent replication of the metabolic result in the records reviewed, and nothing was tested in people.

2018 originating paper: body weight, insulin sensitivity and glucose in obese mice

Animal study

Kannt A et al. Sci Rep. 2018;8(1):3660. PMID 29483571.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

Participants / model
Mice with high fat diet induced obesity; NNMT knockout mice; ob/ob and db/db mice
Treatment
JBSNF-000088; dose, route and duration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (industry authors)
Funding
The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys

The abstract reports body weight, not fat mass. A single originating metabolic paper with industry authors and no independent replication of the metabolic result in the records reviewed.

Read the original source
PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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 JBSNF-000088?

No human safety or toxicology data exist for JBSNF-000088 in the records reviewed. The safety-panel statement in the literature belongs to a different compound, JBSNF-000028, and outside groups report reduced viability in several cancer cell types.

No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it. The statement that a compound was inactive against a broad panel of targets related to metabolism and safety belongs to the different compound JBSNF-000028.

In cell work by outside groups, a 2025 comparison of NNMT inhibitors including 6-methoxynicotinamide found that treated osteosarcoma and Merkel cell carcinoma cells had significantly reduced viability, increased reactive oxygen species and activated apoptotic pathways, and the compound inhibited proliferation of drug-resistant lung cancer cells. These are cell findings, not human safety results.

No pharmacokinetic figures are in the abstracts reviewed. The 2018 abstract reports only that the N-methylated product was detected in plasma of treated mice.

PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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
2022 paper on the sibling compound JBSNF-000028: effect persisted in knockout mice

Animal study

Ruf S et al. Sci Rep. 2022;12(1):15440. PMID 36104373.

A 2022 paper from the same program describes JBSNF-000028, a different tricyclic NNMT inhibitor that reduced MNA in mouse plasma, liver and adipose tissue and drove insulin sensitization, glucose modulation and body weight reduction in a diet-induced obese mouse model. It was inactive against a broad panel of targets related to metabolism and safety. Its improvement in glucose tolerance was also seen in NNMT knockout mice with diet-induced obesity, which the authors say points to a glucose-normalizing effect that may go beyond NNMT inhibition.

Participants / model
Diet-induced obese mice, including NNMT knockout mice (JBSNF-000028)
Treatment
JBSNF-000028; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (different compound)
Funding
not stated in the source

These findings are for JBSNF-000028, not JBSNF-000088. For JBSNF-000088 the 2018 paper reports the opposite pattern, with effects absent in knockout mice, so the specificity evidence differs between the two compounds.

Read the original source
Outside group: lesion weight and number reduced in a mouse endometriosis model

Animal study

Hou S et al. Cell Death Discov. 2024;10(1):463. PMID 39489776.

In a mouse endometriosis model JBSNF-000088 markedly reduced lesion weight and number, and it attenuated proliferation, migration and invasion of endometrial stromal cells.

Participants / model
A mouse endometriosis model; endometrial stromal cells
Treatment
JBSNF-000088 in vivo and in cell culture; in vivo route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study by an outside group
Funding
not stated in the source

Shows outside use of the compound as an NNMT tool. Other outside uses without separate links: drug-resistant lung cancer cells (PMID 40679940), ovarian cancer cell lines (PMID 41511664) and a 2025 comparison of NNMT inhibitors including 6-methoxynicotinamide in which treated osteosarcoma and Merkel cell carcinoma cells had significantly reduced viability, increased reactive oxygen species and activated apoptotic pathways (PMID 41301471). None tests the fat loss claim.

Read the original source
PubMed: 1 record, no exposure, half-life or bioavailability figures

PubMed search record

PubMed search for (JBSNF-000088 OR 6-methoxynicotinamide) AND (pharmacokinetic OR bioavailability OR oral OR plasma), run 10 October 2026.

A PubMed query on 10 October 2026 for JBSNF-000088 or 6-methoxynicotinamide with pharmacokinetic, bioavailability, oral or plasma returned 1 record, the 2018 paper, whose abstract reports only that the N-methylated product was detected in plasma of treated mice. It gives no exposure, half-life, bioavailability or dose figures.

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

An absence finding as of 10 October 2026, based on abstracts. Any pharmacokinetic values would be in the full text, which this page does not summarize.

Read the original source

Why does JBSNF-000088 sit in C tier?

JBSNF-000088 sits with 5-amino-1MQ in C: a plausible mechanism and a body weight and glucose result in diet-induced obese mice, but no human data, no registered study, no pharmacokinetic figures in the abstracts and a single originating paper from industry authors. It is not graded D because nothing reviewed shows a failed trial, poor absorption or documented harm.

5-amino-1MQ, which the site grades C, has the same target and the same kind of evidence. JBSNF-000088 is an NNMT inhibitor with a plausible mechanism and a body weight and glucose result in diet-induced obese mice, but it has no human data, no registered study, no pharmacokinetic figures in the abstracts, and a single originating metabolic paper from industry authors with no independent replication of the metabolic result in the records reviewed.

It is not graded D because nothing reviewed shows a failed trial, poor absorption or documented harm.

2018 originating paper: body weight, insulin sensitivity and glucose in obese mice

Animal study

Kannt A et al. Sci Rep. 2018;8(1):3660. PMID 29483571.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

Participants / model
Mice with high fat diet induced obesity; NNMT knockout mice; ob/ob and db/db mice
Treatment
JBSNF-000088; dose, route and duration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (industry authors)
Funding
The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys

The abstract reports body weight, not fat mass. A single originating metabolic paper with industry authors and no independent replication of the metabolic result in the records reviewed.

Read the original source
PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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
PubMed: 1 record, no exposure, half-life or bioavailability figures

PubMed search record

PubMed search for (JBSNF-000088 OR 6-methoxynicotinamide) AND (pharmacokinetic OR bioavailability OR oral OR plasma), run 10 October 2026.

A PubMed query on 10 October 2026 for JBSNF-000088 or 6-methoxynicotinamide with pharmacokinetic, bioavailability, oral or plasma returned 1 record, the 2018 paper, whose abstract reports only that the N-methylated product was detected in plasma of treated mice. It gives no exposure, half-life, bioavailability or dose figures.

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

An absence finding as of 10 October 2026, based on abstracts. Any pharmacokinetic values would be in the full text, which this page does not summarize.

Read the original source

Studies and sources

PubChem: 6-methoxynicotinamide, JBSNF-000088 listed as a synonym

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 250810, 6-methoxypyridine-3-carboxamide.

JBSNF-000088 is listed as a synonym on PubChem CID 250810, 6-methoxypyridine-3-carboxamide (6-methoxynicotinamide), C7H8N2O2, 152.15 g/mol, CAS 7150-23-4. The 2018 paper describes it as a small molecule analog of nicotinamide.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined small molecule, no salt form
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. JBSNF-000028, a related compound from the same program, is a different tricyclic molecule and is not the same material.

Read the original source
2018 originating paper: body weight, insulin sensitivity and glucose in obese mice

Animal study

Kannt A et al. Sci Rep. 2018;8(1):3660. PMID 29483571.

JBSNF-000088 inhibited NNMT activity and reduced 1-methyl-nicotinamide (MNA) levels. In mice with high fat diet induced obesity it reduced body weight, improved insulin sensitivity, and normalized glucose tolerance to the level of lean control mice. These effects were not seen in NNMT knockout mice on the high fat diet, which the authors take as evidence of specificity. In ob/ob and db/db mice it improved glucose handling to a lesser extent and without weight loss. A co-crystal structure showed the N-methylated product of JBSNF-000088 bound to NNMT, and that product was detected in plasma of treated mice, so the authors suggest it acts as a slow-turnover substrate analog.

Participants / model
Mice with high fat diet induced obesity; NNMT knockout mice; ob/ob and db/db mice
Treatment
JBSNF-000088; dose, route and duration not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (industry authors)
Funding
The authors are employees of Sanofi-Aventis Deutschland and Jubilant Biosys

The abstract reports body weight, not fat mass. A single originating metabolic paper with industry authors and no independent replication of the metabolic result in the records reviewed.

Read the original source
2018 paper on a different NNMT inhibitor class: context for the target only

Animal study

Neelakantan H et al. Biochem Pharmacol. 2018;147:141-152. PMID 29155147.

A 2018 paper on methylquinolinium NNMT inhibitors reported that treating diet-induced obese mice systemically with a potent NNMT inhibitor significantly reduced body weight and white adipose mass, decreased adipocyte size, and lowered plasma total cholesterol, with no change in total food intake and no observable adverse effects. In cultured adipocytes the inhibitors reduced 1-MNA, raised NAD+ and SAM, and suppressed lipogenesis.

Participants / model
Diet-induced obese mice; cultured adipocytes
Treatment
A potent methylquinolinium NNMT inhibitor given systemically; the compound, dose and route are not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (different chemistry)
Funding
not stated in the source

The abstract does not name the compound dosed in mice, so this paper is context for the target, not evidence for JBSNF-000088, and it does not by itself make any claim about 5-amino-1MQ.

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2022 paper on the sibling compound JBSNF-000028: effect persisted in knockout mice

Animal study

Ruf S et al. Sci Rep. 2022;12(1):15440. PMID 36104373.

A 2022 paper from the same program describes JBSNF-000028, a different tricyclic NNMT inhibitor that reduced MNA in mouse plasma, liver and adipose tissue and drove insulin sensitization, glucose modulation and body weight reduction in a diet-induced obese mouse model. It was inactive against a broad panel of targets related to metabolism and safety. Its improvement in glucose tolerance was also seen in NNMT knockout mice with diet-induced obesity, which the authors say points to a glucose-normalizing effect that may go beyond NNMT inhibition.

Participants / model
Diet-induced obese mice, including NNMT knockout mice (JBSNF-000028)
Treatment
JBSNF-000028; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study (different compound)
Funding
not stated in the source

These findings are for JBSNF-000028, not JBSNF-000088. For JBSNF-000088 the 2018 paper reports the opposite pattern, with effects absent in knockout mice, so the specificity evidence differs between the two compounds.

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Outside group: lesion weight and number reduced in a mouse endometriosis model

Animal study

Hou S et al. Cell Death Discov. 2024;10(1):463. PMID 39489776.

In a mouse endometriosis model JBSNF-000088 markedly reduced lesion weight and number, and it attenuated proliferation, migration and invasion of endometrial stromal cells.

Participants / model
A mouse endometriosis model; endometrial stromal cells
Treatment
JBSNF-000088 in vivo and in cell culture; in vivo route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study by an outside group
Funding
not stated in the source

Shows outside use of the compound as an NNMT tool. Other outside uses without separate links: drug-resistant lung cancer cells (PMID 40679940), ovarian cancer cell lines (PMID 41511664) and a 2025 comparison of NNMT inhibitors including 6-methoxynicotinamide in which treated osteosarcoma and Merkel cell carcinoma cells had significantly reduced viability, increased reactive oxygen species and activated apoptotic pathways (PMID 41301471). None tests the fat loss claim.

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Outside group: tumor development compromised in gallbladder carcinoma xenografts

Animal study

Li Y et al. Hepatology. 2023;78(5):1352-1367. PMID 36633260.

In xenografted gallbladder carcinoma models overexpressing NNMT, JBSNF-000088 compromised tumor development and altered immune marker expression.

Participants / model
Xenografted gallbladder carcinoma models overexpressing NNMT
Treatment
JBSNF-000088; route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study by an outside group
Funding
not stated in the source

Shows outside use of the compound as an NNMT tool. It does not test the fat loss claim.

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PubMed: 0 trial-type records for NNMT inhibitors; 6 JBSNF records, all mouse or cell work

PubMed search record

PubMed search for JBSNF[tiab] OR JBSNF-000088[tiab] OR JBSNF-000028[tiab], run 10 October 2026, with a clinical trial filter query for NNMT inhibitors, ClinicalTrials.gov and DailyMed queries.

A PubMed query on 10 October 2026 for NNMT or nicotinamide N-methyltransferase with inhibitor and clinical trial, randomized controlled trial or controlled clinical trial publication types returned 0 records. A query for JBSNF[tiab] or JBSNF-000088[tiab] or JBSNF-000028[tiab] returned 6 records, all mouse or cell work or tool use. ClinicalTrials.gov queries for JBSNF-000088, 6-methoxynicotinamide and NNMT inhibitor returned no studies, and DailyMed returned no label for either name. No abstract reviewed reports JBSNF-000088 given to a person or any toxicology result for it.

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.

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Why is JBSNF-000088 in C tier?

C fits an NNMT inhibitor with a plausible mechanism and a body weight and glucose result in diet-induced obese mice, graded alongside 5-amino-1MQ, which shares the target and the kind of evidence. It has no human data, no registered study, no pharmacokinetic figures in the abstracts and a single originating paper from industry authors. It is not graded D because nothing reviewed shows a failed trial, poor absorption or documented harm.