DADA

updated

DADA is diisopropylammonium dichloroacetate, a different salt from the sodium dichloroacetate used in nearly all clinical dichloroacetate research. The only controlled human trial of DADA itself located compared two doses in 123 Chinese patients with fatty liver and had no placebo arm, and a PubMed search on 9 October 2026 found no study of it in healthy people, for performance or body composition, or by any injected route. Dichloroacetate trials missed most clinical endpoints, and one stopped early for peripheral neuropathy, a finding no source ties to DADA.

Dichloroacetate salt of diisopropylamine

  • DADA is PubChem CID 12617 (C8H17Cl2NO2, 230.13 g/mol); it shares only the dichloroacetate anion with sodium dichloroacetate, the salt used in nearly all clinical dichloroacetate research.
  • No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and a DailyMed search for dichloroacetate on 9 October 2026 returned no labels.
  • The only controlled human trial of DADA itself located compared two doses in 123 Chinese patients with nonalcoholic fatty liver disease over 8 weeks and had no placebo arm.
  • In the Ames test, both DADA and diisopropylamine alone were mutagenic; no human carcinogenicity data were located.
  • A randomized trial of dichloroacetate in MELAS was terminated early for peripheral nerve toxicity (17 of 19 patients discontinued); that is a dichloroacetate finding, not shown for DADA.
  • A PubMed search on 9 October 2026 returned 10 records for DADA with exercise, performance, injection and related terms; none studied DADA in humans for performance, body composition or any injected route.

What is DADA, and is it approved?

DADA is diisopropylammonium dichloroacetate, a salt of dichloroacetic acid with diisopropylamine. It shares only its anion with the sodium dichloroacetate used in nearly all clinical dichloroacetate research. No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and DailyMed returned no dichloroacetate label on 9 October 2026.

DADA is PubChem CID 12617 (C8H17Cl2NO2, molecular weight 230.13 g/mol, CAS 660-27-5). Listed synonyms include diisopropylamine dichloroacetate, Dipromonium, Kalodil, Oxypangam and IS-401. It is a salt of dichloroacetic acid with diisopropylamine, so it dissociates into two moieties.

Dichloroacetic acid itself is CID 6597 (C2H2Cl2O2, 128.94 g/mol, CAS 79-43-6). The salt used in nearly all of the clinical dichloroacetate research is sodium dichloroacetate (CID 517326, C2HCl2NaO2, 150.92 g/mol, CAS 2156-56-1). DADA and sodium dichloroacetate share an anion and nothing else, and the diisopropylamine half has its own pharmacology. Every dichloroacetate trial on this page is labeled as dichloroacetate or sodium dichloroacetate, not DADA.

In a proposed rule published on 5 September 2019 (84 FR 46688), FDA evaluated sodium dichloroacetate for the section 503A compounding bulks list and proposed not to include it. The notice cites significant safety concerns primarily related to its toxicity profile in nonclinical and clinical studies, one identified study closed due to patient deaths and safety concerns, no evidence that it would be effective in preventing or treating cancer, and no evidence of historical use in compounded drug products. The Pharmacy Compounding Advisory Committee voted not to include it at its 23 June 2016 meeting. The current eCFR text of 21 CFR 216.23, read for the 1 October 2026 edition, lists sodium dichloroacetate neither among the substances that can be used nor among those formally determined not to be included, so the 2019 proposal has not been codified.

No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and a DailyMed search for dichloroacetate on 9 October 2026 returned no labels. Approvals and marketing outside the United States are not covered.

PubChem: DADA identity and how it differs from sodium dichloroacetate

Chemical identity record

National Library of Medicine. PubChem compound records CID 12617 (diisopropylammonium dichloroacetate), CID 6597 (dichloroacetic acid) and CID 517326 (sodium dichloroacetate).

DADA, diisopropylammonium dichloroacetate: PubChem CID 12617, C8H17Cl2NO2, molecular weight 230.13 g/mol, CAS 660-27-5; listed synonyms include diisopropylamine dichloroacetate, Dipromonium, Kalodil, Oxypangam and IS-401. It is a salt of dichloroacetic acid with diisopropylamine, so it dissociates into two moieties. Dichloroacetic acid itself is CID 6597, C2H2Cl2O2, 128.94 g/mol, CAS 79-43-6. The salt used in nearly all of the clinical dichloroacetate research is sodium dichloroacetate, CID 517326, C2HCl2NaO2, 150.92 g/mol, CAS 2156-56-1. DADA and sodium dichloroacetate share an anion and nothing else, and the diisopropylamine half has its own pharmacology.

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

Identity record only. The distinction between DADA and sodium dichloroacetate is the point of the record: findings for one are not findings for the other.

Read the original source
FDA 503A proposed rule, 5 September 2019: sodium dichloroacetate not proposed for the bulks list

Regulatory record

U.S. Food and Drug Administration. Amendments to the List of Bulk Drug Substances That Can Be Used To Compound Drug Products in Accordance With Section 503A of the Federal Food, Drug, and Cosmetic Act. Proposed rule, Federal Register, 5 September 2019, 84 FR 46688. Current 21 CFR 216.23 read for the 1 October 2026 eCFR edition.

In a proposed rule published on 5 September 2019 (84 FR 46688), FDA evaluated sodium dichloroacetate for the section 503A compounding bulks list and proposed not to include it, stating significant safety concerns primarily related to its toxicity profile in nonclinical and clinical studies, that one identified study was closed due to patient deaths and safety concerns, that there is no evidence it would be effective in preventing or treating cancer, and that no evidence of historical use in compounded drug products was found. The Pharmacy Compounding Advisory Committee voted not to include it at its 23 June 2016 meeting. The current eCFR text of 21 CFR 216.23, read for the 1 October 2026 edition, lists sodium dichloroacetate neither among the substances that can be used nor among those formally determined not to be included, so the 2019 proposal has not been codified. No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and a DailyMed search for dichloroacetate on 9 October 2026 returned no labels.

Participants / model
FDA compounding evaluation, not a clinical population
Treatment
Bulk drug substance
Follow-up
Proposed rule of 5 September 2019; eCFR read for the 1 October 2026 edition
Study design
Federal Register proposed rule and current codified text
Funding
not stated in the source

The rule concerns sodium dichloroacetate, the anion's usual salt, not DADA. It is a proposal and has not been codified.

Read the original source

Does a product labeled pangamic acid or vitamin B15 contain DADA?

Not necessarily. A 1999 analytical study found three separate substances in German market products declared as pangamic acid: gluconic acid, glycine and diisopropylammonium dichloroacetate. A label saying pangamic acid or vitamin B15 does not identify the molecule inside.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate.

The one controlled human performance study carried out under the pangamic acid name tested a different chemical entirely. In a double-blind study, 16 male track athletes took pangamic acid tablets, stated in the paper as calcium gluconate and N,N-dimethylglycine, or placebo for three weeks and were tested on the Bruce treadmill protocol. MANOVA found no significant differences between groups after treatment in maximal heart rate, treadmill time, recovery heart rate, or post-test blood glucose and lactate. This is a null result, and it is a null result for a product that did not contain DADA.

1999 analytical study: pangamic acid products held gluconic acid, glycine or DADA

Chemical identity record

Schneider D et al. Arzneimittelforschung. 1999;49(4):335-43. PMID 10337453.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate. The authors also report that high concentrations of DIPA deteriorated mitochondrial respiratory control in vitro by increasing state IV oxygen consumption.

Participants / model
Commercial products and isolated mitochondria
Treatment
Marketed oral products; in vitro exposure
Follow-up
Not applicable
Study design
Original analytical and mechanistic study
Funding
not stated in the source

A product label saying pangamic acid or vitamin B15 does not identify the molecule inside. The mitochondrial result is in vitro.

Read the original source
Pangamic acid trial: 16 male track athletes, null result, product did not contain DADA

Clinical trial

Gray ME et al. Med Sci Sports Exerc. 1982;14(6):424-7. PMID 7162387.

In a double-blind study, 16 male track athletes took pangamic acid tablets, stated in the paper as calcium gluconate and N,N-dimethylglycine, or placebo for three weeks and were tested on the Bruce treadmill protocol. MANOVA found no significant differences between groups after treatment in maximal heart rate, treadmill time, recovery heart rate, or post-test blood glucose and lactate.

Participants / model
16 male track athletes
Treatment
Oral tablets of calcium gluconate plus dimethylglycine, or placebo (dose not reproduced on this page)
Follow-up
3 weeks
Study design
Double-blind placebo-controlled study
Funding
not stated in the source

The one controlled human performance study carried out under the pangamic acid name tested a different chemical entirely. It is a null result for a product that did not contain DADA.

Read the original source

What has been tested in people for DADA itself?

One randomized dose-comparison trial: 127 enrolled and 123 analyzed Chinese patients with nonalcoholic fatty liver disease over 8 weeks, with no placebo arm. It cannot show efficacy against no treatment, and no study tests DADA in healthy people, for weight, performance or body composition, or by any injected route.

The only controlled human trial of DADA itself located in the records reviewed was a randomized double-blind dose-parallel trial in China. It enrolled 127 patients with nonalcoholic fatty liver disease, randomized them to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, and analyzed 123 after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%). There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

A PubMed search on 9 October 2026 for diisopropylamine or diisopropylammonium dichloroacetate with exercise, performance, athletes, bodybuilding, injection, injectable, intramuscular or subcutaneous returned 10 records. None studied DADA in humans for performance, body composition or any injected route. They covered poultry liver morphology, insect gene editing, a doping-control assay for diisopropylamine in horse urine, two mouse tumor xenograft studies, a rat steatohepatitis herbal study, a postoperative pain scale, a rat teratology study of an unrelated compound, a cholinesterase enzymology paper, and a 1963 report of intracarotid injection in vascular patients. No human efficacy, pharmacokinetic or safety data exist for any injected DADA preparation in the records reviewed.

DADA in fatty liver: 127 enrolled, 123 analyzed, two doses, no placebo arm

Clinical trial

Lu LG et al. Zhonghua Gan Zang Bing Za Zhi. 2005;13(2):92-5. PMID 15727691.

A randomized double-blind dose-parallel trial in China enrolled 127 patients with nonalcoholic fatty liver disease, randomized to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, with 123 analyzed after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%).

Participants / model
127 enrolled, 123 analyzed, patients with nonalcoholic fatty liver disease
Treatment
Oral diisopropylamine dichloroacetate at two daily dose levels for 8 weeks (doses not reproduced on this page)
Follow-up
8 weeks
Study design
Randomized double-blind dose-comparison trial with no placebo arm
Funding
not stated in the source

The only controlled human trial of DADA itself located. There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

Read the original source
PubMed search, 9 October 2026: 10 records, none on performance, body composition or injection

PubMed search record

PubMed search run on 9 October 2026: (diisopropylamine dichloroacetate OR diisopropylammonium dichloroacetate) AND (exercise OR performance OR athletes OR bodybuilding OR injection OR injectable OR intramuscular OR subcutaneous). 10 records returned.

The search returned 10 records. None studied DADA in humans for performance, body composition or any injected route. They covered poultry liver morphology, insect gene editing, a doping-control assay for diisopropylamine in horse urine, two mouse tumor xenograft studies, a rat steatohepatitis herbal study, a postoperative pain scale, a rat teratology study of an unrelated compound, a cholinesterase enzymology paper, and a 1963 report of intracarotid injection in vascular patients. No human efficacy, pharmacokinetic or safety data exist for any injected DADA preparation in the records reviewed.

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

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

Read the original source

What do dichloroacetate trials show, and do they apply to DADA?

They concern dichloroacetate, given as sodium dichloroacetate where the source names the salt, and none is a DADA result. Lactate fell in several trials, clinical endpoints were mostly missed, and a randomized MELAS trial stopped early because 17 of 19 patients discontinued for peripheral neuropathy.

The Dichloroacetate-Lactic Acidosis Study Group randomized 252 adults with lactic acidosis (blood lactate at least 5.0 mmol/L with pH at most 7.35 or a base deficit of at least 6 mmol/L) to intravenous sodium dichloroacetate or placebo, 126 each. Lactate fell by 20% or more in 66% on dichloroacetate versus 36% on placebo (P = 0.001) and arterial pH rose more (P = 0.005), but the absolute differences were small and there was no improvement in hemodynamics or survival: 12% of dichloroacetate patients and 17% of placebo patients survived to hospital discharge. The authors call the changes statistically significant but clinically unimportant.

A double-blind randomized controlled trial in 43 children aged 0.9 to 19 years with congenital lactic acidosis gave oral dichloroacetate or placebo for 6 months after a 6-month placebo preconditioning period. There were no significant differences in global assessment of treatment efficacy scores, linear growth, or frequency or severity of intercurrent illnesses. Dichloroacetate significantly decreased the rise in blood lactate after carbohydrate feeding.

A 2026 phase III multicenter trial in 34 children with pyruvate dehydrogenase complex deficiency randomized participants to 4 months of sodium dichloroacetate or placebo, then a 1-month washout and crossover, with an optional open-label extension. The primary endpoint, the observer-reported outcomes motor domain score, was not significantly different between treatment and placebo (P = 0.512). Longer-term treatment including the open-label extension showed a significant treatment effect (P = 0.002), strongest in participants with higher baseline motor impairment (P = 0.001). Plasma lactate fell 0.48 (SD 0.82) mmol/L, 20%, P = 0.006, and survival exceeded a natural history cohort (log-rank P = 0.027). Chronic dosing was described as well tolerated and safe. Several authors have financial interests in the sponsor or the study drug.

A double-blind placebo-controlled randomized 3-year crossover trial of dichloroacetate in 30 patients aged 10 to 60 with MELAS and the A3243G mutation was terminated early for peripheral nerve toxicity. During the initial 24-month treatment period, 15 of 15 patients randomized to dichloroacetate were taken off study medication versus 4 of 15 on placebo, and study medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. The mean global assessment score did not differ between arms.

None of these trials tested DADA, so no result applies to it.

Sodium dichloroacetate in lactic acidosis: 252 adults, lactate fell, survival did not change (not DADA)

Randomized controlled trial

Stacpoole PW et al. N Engl J Med. 1992;327(22):1564-9. PMID 1435883.

The Dichloroacetate-Lactic Acidosis Study Group randomized 252 adults with lactic acidosis (blood lactate at least 5.0 mmol/L with pH at most 7.35 or a base deficit of at least 6 mmol/L) to intravenous sodium dichloroacetate or placebo, 126 each. Lactate fell by 20% or more in 66% on dichloroacetate versus 36% on placebo (P = 0.001) and arterial pH rose more (P = 0.005), but the absolute differences were small and there was no improvement in hemodynamics or survival: 12% of dichloroacetate patients and 17% of placebo patients survived to hospital discharge. The authors call the changes statistically significant but clinically unimportant.

Participants / model
252 critically ill adults with lactic acidosis
Treatment
Intravenous sodium dichloroacetate or placebo
Follow-up
not stated in the source
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

This is sodium dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Dichloroacetate in congenital lactic acidosis: 43 children, no clinical benefit (not DADA)

Randomized controlled trial

Stacpoole PW et al. Pediatrics. 2006;117(5):1519-31. PMID 16651305.

A double-blind randomized controlled trial in 43 children aged 0.9 to 19 years with congenital lactic acidosis gave oral dichloroacetate or placebo for 6 months after a 6-month placebo preconditioning period. There were no significant differences in global assessment of treatment efficacy scores, linear growth, or frequency or severity of intercurrent illnesses. Dichloroacetate significantly decreased the rise in blood lactate after carbohydrate feeding. Chronic administration was associated with a fall in plasma clearance of the drug and a rise in urinary maleylacetone and delta-aminolevulinate.

Participants / model
43 children with congenital lactic acidosis
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
6 months after a 6-month placebo preconditioning period
Study design
Randomized double-blind placebo-controlled trial
Funding
not stated in the source

This is dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Sodium dichloroacetate phase 3, 2026: 34 children, primary endpoint missed (not DADA)

Randomized controlled trial

Stacpoole PW et al. JCI Insight. 2026;11(18). PMID 42770298.

A 2026 phase III multicenter trial in 34 children with pyruvate dehydrogenase complex deficiency randomized participants to 4 months of sodium dichloroacetate or placebo, then a 1-month washout and crossover, with an optional open-label extension, dosing set by GSTZ1 pharmacogenomic haplotype. The primary endpoint, the observer-reported outcomes motor domain score, was not significantly different between treatment and placebo (P = 0.512). Longer-term treatment including the open-label extension showed a significant treatment effect (P = 0.002), strongest in participants with higher baseline motor impairment (P = 0.001). Plasma lactate fell 0.48 (SD 0.82) mmol/L, 20%, P = 0.006, and survival exceeded a natural history cohort (log-rank P = 0.027). Chronic dosing was described as well tolerated and safe.

Participants / model
34 children with pyruvate dehydrogenase complex deficiency
Treatment
Oral sodium dichloroacetate, dose set by GSTZ1 haplotype, or placebo
Follow-up
4 months, 1-month washout and crossover, optional open-label extension
Study design
Randomized double-blind phase 3 trial with crossover and open-label extension
Funding
Several authors have financial interests in the sponsor or the study drug.

This is sodium dichloroacetate, not DADA. The primary endpoint was missed, and the effect appeared only with longer treatment including the open-label extension.

Read the original source
Dichloroacetate in MELAS: 30 patients, stopped early for peripheral neuropathy (not DADA)

Randomized controlled trial

Kaufmann P et al. Neurology. 2006;66(3):324-30. PMID 16476929.

A double-blind placebo-controlled randomized 3-year crossover trial of dichloroacetate in 30 patients aged 10 to 60 with MELAS and the A3243G mutation was terminated early for peripheral nerve toxicity. During the initial 24-month treatment period, 15 of 15 patients randomized to dichloroacetate were taken off study medication versus 4 of 15 on placebo, and study medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. The mean global assessment score did not differ between arms.

Participants / model
30 patients aged 10 to 60 with MELAS
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
Planned 3 years; terminated early
Study design
Randomized double-blind placebo-controlled crossover trial
Funding
not stated in the source

Peripheral neuropathy is a dichloroacetate finding with this trial attached. No source ties it to DADA.

Read the original source

Does DADA work because dichloroacetate research exists?

No. The supplier's description, a dichloroacetate salt with a complicated history, is accurate, and the history is the whole record. DADA has not been studied in healthy people, for performance or body composition, or by any injected route, and the dichloroacetate results belong to a different salt.

The claim being tested is that DADA is a dichloroacetate salt with a complicated history, sold on the strength of dichloroacetate research. The naming tangle is documented: a pangamic acid or vitamin B15 label does not identify the molecule inside, and the dichloroacetate trials used dichloroacetate or sodium dichloroacetate, not DADA.

On DADA itself the record is one 8-week two-dose comparison in 123 Chinese patients with fatty liver and no placebo arm, an Ames test in which both the salt and the amine were mutagenic, and a mouse influenza model with supplier ties. Nothing has been studied for the salt in healthy people, for performance, for body composition or by any injected route.

1999 analytical study: pangamic acid products held gluconic acid, glycine or DADA

Chemical identity record

Schneider D et al. Arzneimittelforschung. 1999;49(4):335-43. PMID 10337453.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate. The authors also report that high concentrations of DIPA deteriorated mitochondrial respiratory control in vitro by increasing state IV oxygen consumption.

Participants / model
Commercial products and isolated mitochondria
Treatment
Marketed oral products; in vitro exposure
Follow-up
Not applicable
Study design
Original analytical and mechanistic study
Funding
not stated in the source

A product label saying pangamic acid or vitamin B15 does not identify the molecule inside. The mitochondrial result is in vitro.

Read the original source
DADA in fatty liver: 127 enrolled, 123 analyzed, two doses, no placebo arm

Clinical trial

Lu LG et al. Zhonghua Gan Zang Bing Za Zhi. 2005;13(2):92-5. PMID 15727691.

A randomized double-blind dose-parallel trial in China enrolled 127 patients with nonalcoholic fatty liver disease, randomized to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, with 123 analyzed after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%).

Participants / model
127 enrolled, 123 analyzed, patients with nonalcoholic fatty liver disease
Treatment
Oral diisopropylamine dichloroacetate at two daily dose levels for 8 weeks (doses not reproduced on this page)
Follow-up
8 weeks
Study design
Randomized double-blind dose-comparison trial with no placebo arm
Funding
not stated in the source

The only controlled human trial of DADA itself located. There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

Read the original source
Ames test: both DADA and diisopropylamine alone were mutagenic

Cell study

Gelernt MD et al. Nutr Cancer. 1982;3(3):129-33. PMID 6752894.

In the Ames Salmonella mammalian microsome mutagenicity test, both diisopropylamine dichloroacetate and diisopropylamine alone demonstrated mutagenicity. The authors note that 90% of such agents prove carcinogenic and that this must be considered in any proposed use of pangamic acid containing either substance.

Participants / model
Salmonella strains with mammalian microsomal activation
Treatment
In vitro exposure
Follow-up
Not applicable
Study design
Original in vitro toxicology study
Funding
not stated in the source

This is a bacterial assay, not a human finding, and no human carcinogenicity data were located.

Read the original source
Mouse influenza model: oral DADA restored PDH activity and ATP; supplier ties

Animal study

Yamane K et al. PLoS One. 2014;9(5):e98032. PMID 24865588.

Mice infected with influenza A PR/8/34 (H1N1) showed down-regulated pyruvate dehydrogenase activity and ATP, with up-regulated PDK4 in skeletal muscle, heart, liver and lungs. Oral DADA at 12-hour intervals for 14 days restored PDH activity and ATP, improved glucose and lipid metabolism, improved survival, and suppressed cytokine responses and viral replication. DADA is characterized here as a PDK4 inhibitor.

Participants / model
Mice infected with influenza A H1N1
Treatment
Oral DADA every 12 hours for 14 days; dose not stated in the source
Follow-up
14 days
Study design
Original animal infection study
Funding
Two authors were employed by the company that supplied the compound, and five are inventors on a patent application covering it for influenza.

This is a mouse infection model and supports no human claim.

Read the original source
PubMed search, 9 October 2026: 10 records, none on performance, body composition or injection

PubMed search record

PubMed search run on 9 October 2026: (diisopropylamine dichloroacetate OR diisopropylammonium dichloroacetate) AND (exercise OR performance OR athletes OR bodybuilding OR injection OR injectable OR intramuscular OR subcutaneous). 10 records returned.

The search returned 10 records. None studied DADA in humans for performance, body composition or any injected route. They covered poultry liver morphology, insect gene editing, a doping-control assay for diisopropylamine in horse urine, two mouse tumor xenograft studies, a rat steatohepatitis herbal study, a postoperative pain scale, a rat teratology study of an unrelated compound, a cholinesterase enzymology paper, and a 1963 report of intracarotid injection in vascular patients. No human efficacy, pharmacokinetic or safety data exist for any injected DADA preparation in the records reviewed.

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

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

Read the original source

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

In a mouse influenza model, oral DADA, characterized as a PDK4 inhibitor, restored pyruvate dehydrogenase activity and ATP and improved survival, which supports no human claim. No human pharmacokinetics for DADA were found, and the diisopropylamine half is a banned substance in equine racing.

DADA is a salt of dichloroacetic acid with diisopropylamine, so it dissociates into two moieties. It shares only its anion with sodium dichloroacetate, and the diisopropylamine half has its own pharmacology.

Mice infected with influenza A PR/8/34 (H1N1) showed down-regulated pyruvate dehydrogenase activity and ATP, with up-regulated PDK4 in skeletal muscle, heart, liver and lungs. Oral DADA at 12-hour intervals for 14 days restored PDH activity and ATP, improved glucose and lipid metabolism, improved survival, and suppressed cytokine responses and viral replication. DADA is characterized there as a PDK4 inhibitor. Two authors were employed by the company that supplied the compound and five are inventors on a patent application covering it for influenza. This is a mouse infection model and supports no human claim.

A horse racing laboratory paper states that diisopropylamine is used as an intravenous antihypertensive agent and is prohibited in the horse racing industry because of performance enhancing effects. It reports an N-oxidized metabolite of diisopropylamine, produced mainly by flavin-containing monooxygenase, in an actual horse urine sample that tested positive. This establishes that the diisopropylamine half is a banned substance in equine racing with a detection method behind it. It is not a human performance result, and the paper reports none.

In isolated mitochondria, the 1999 analytical study reported that high concentrations of diisopropylamine deteriorated mitochondrial respiratory control by increasing state IV oxygen consumption. That is an in vitro finding. The records reviewed give no human pharmacokinetics for DADA.

PubChem: DADA identity and how it differs from sodium dichloroacetate

Chemical identity record

National Library of Medicine. PubChem compound records CID 12617 (diisopropylammonium dichloroacetate), CID 6597 (dichloroacetic acid) and CID 517326 (sodium dichloroacetate).

DADA, diisopropylammonium dichloroacetate: PubChem CID 12617, C8H17Cl2NO2, molecular weight 230.13 g/mol, CAS 660-27-5; listed synonyms include diisopropylamine dichloroacetate, Dipromonium, Kalodil, Oxypangam and IS-401. It is a salt of dichloroacetic acid with diisopropylamine, so it dissociates into two moieties. Dichloroacetic acid itself is CID 6597, C2H2Cl2O2, 128.94 g/mol, CAS 79-43-6. The salt used in nearly all of the clinical dichloroacetate research is sodium dichloroacetate, CID 517326, C2HCl2NaO2, 150.92 g/mol, CAS 2156-56-1. DADA and sodium dichloroacetate share an anion and nothing else, and the diisopropylamine half has its own pharmacology.

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

Identity record only. The distinction between DADA and sodium dichloroacetate is the point of the record: findings for one are not findings for the other.

Read the original source
Mouse influenza model: oral DADA restored PDH activity and ATP; supplier ties

Animal study

Yamane K et al. PLoS One. 2014;9(5):e98032. PMID 24865588.

Mice infected with influenza A PR/8/34 (H1N1) showed down-regulated pyruvate dehydrogenase activity and ATP, with up-regulated PDK4 in skeletal muscle, heart, liver and lungs. Oral DADA at 12-hour intervals for 14 days restored PDH activity and ATP, improved glucose and lipid metabolism, improved survival, and suppressed cytokine responses and viral replication. DADA is characterized here as a PDK4 inhibitor.

Participants / model
Mice infected with influenza A H1N1
Treatment
Oral DADA every 12 hours for 14 days; dose not stated in the source
Follow-up
14 days
Study design
Original animal infection study
Funding
Two authors were employed by the company that supplied the compound, and five are inventors on a patent application covering it for influenza.

This is a mouse infection model and supports no human claim.

Read the original source
Horse racing laboratory: diisopropylamine is a banned substance with a detection method

Chemical identity record

Kwak YB et al. J Pharm Biomed Anal. 2023;234:115576. PMID 37459832.

A horse racing laboratory paper states that diisopropylamine is used as an intravenous antihypertensive agent and is prohibited in the horse racing industry because of performance enhancing effects, and reports identifying an N-oxidized metabolite of DIPA, produced mainly by flavin-containing monooxygenase, in an actual horse urine sample that tested positive for DIPA.

Participants / model
Horse urine samples and in vitro liver preparations
Treatment
Not stated for the positive sample; in vitro for the metabolism work
Follow-up
Not applicable
Study design
Original analytical study for doping control
Funding
not stated in the source

This establishes that the diisopropylamine half is a banned substance in equine racing with a detection method behind it. It is not a human performance result, and the paper reports none.

Read the original source
1999 analytical study: pangamic acid products held gluconic acid, glycine or DADA

Chemical identity record

Schneider D et al. Arzneimittelforschung. 1999;49(4):335-43. PMID 10337453.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate. The authors also report that high concentrations of DIPA deteriorated mitochondrial respiratory control in vitro by increasing state IV oxygen consumption.

Participants / model
Commercial products and isolated mitochondria
Treatment
Marketed oral products; in vitro exposure
Follow-up
Not applicable
Study design
Original analytical and mechanistic study
Funding
not stated in the source

A product label saying pangamic acid or vitamin B15 does not identify the molecule inside. The mitochondrial result is in vitro.

Read the original source

What risks does DADA carry?

Safety in people is not established for DADA. Both DADA and diisopropylamine alone were mutagenic in the Ames test, a bacterial finding with no human carcinogenicity data. Peripheral neuropathy is a dichloroacetate finding with its trial attached, and no source ties it to DADA.

In the Ames Salmonella mammalian microsome mutagenicity test, both diisopropylamine dichloroacetate and diisopropylamine alone demonstrated mutagenicity. The authors note that 90% of such agents prove carcinogenic and that this must be considered in any proposed use of pangamic acid containing either substance. This is a bacterial assay, not a human finding, and no human carcinogenicity data were located.

Peripheral neuropathy is a dichloroacetate finding. A randomized crossover trial of dichloroacetate in 30 patients with MELAS was terminated early for peripheral nerve toxicity: 15 of 15 patients on dichloroacetate were taken off study medication in the first 24 months versus 4 of 15 on placebo, and medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. No source ties neuropathy to DADA.

Long-term dichloroacetate data come from 8 patients with pyruvate dehydrogenase complex or respiratory chain deficiencies treated for 9.7 to 16.5 years. Hematological, electrolyte, renal and hepatic status remained stable and blood lactate stayed normal. Nerve conduction either did not change or decreased modestly, leading to dose reduction or temporary discontinuation in 3 of the 8, although symptomatic worsening of peripheral neuropathy did not occur. Dosing was set by weight in a monitored metabolic clinic, which is not how a supplement is taken. In the 43-child trial, chronic administration was associated with a fall in plasma clearance of dichloroacetate and a rise in urinary maleylacetone and delta-aminolevulinate.

FDA's 2019 proposed rule cited significant safety concerns primarily related to the toxicity profile of sodium dichloroacetate and one identified study closed due to patient deaths and safety concerns. It concerns the sodium salt, not DADA, and has not been codified. For DADA itself, the one 8-week two-dose trial reported dry mouth in 1 patient per group (1.6%) and had no placebo arm.

Ames test: both DADA and diisopropylamine alone were mutagenic

Cell study

Gelernt MD et al. Nutr Cancer. 1982;3(3):129-33. PMID 6752894.

In the Ames Salmonella mammalian microsome mutagenicity test, both diisopropylamine dichloroacetate and diisopropylamine alone demonstrated mutagenicity. The authors note that 90% of such agents prove carcinogenic and that this must be considered in any proposed use of pangamic acid containing either substance.

Participants / model
Salmonella strains with mammalian microsomal activation
Treatment
In vitro exposure
Follow-up
Not applicable
Study design
Original in vitro toxicology study
Funding
not stated in the source

This is a bacterial assay, not a human finding, and no human carcinogenicity data were located.

Read the original source
Dichloroacetate in MELAS: 30 patients, stopped early for peripheral neuropathy (not DADA)

Randomized controlled trial

Kaufmann P et al. Neurology. 2006;66(3):324-30. PMID 16476929.

A double-blind placebo-controlled randomized 3-year crossover trial of dichloroacetate in 30 patients aged 10 to 60 with MELAS and the A3243G mutation was terminated early for peripheral nerve toxicity. During the initial 24-month treatment period, 15 of 15 patients randomized to dichloroacetate were taken off study medication versus 4 of 15 on placebo, and study medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. The mean global assessment score did not differ between arms.

Participants / model
30 patients aged 10 to 60 with MELAS
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
Planned 3 years; terminated early
Study design
Randomized double-blind placebo-controlled crossover trial
Funding
not stated in the source

Peripheral neuropathy is a dichloroacetate finding with this trial attached. No source ties it to DADA.

Read the original source
Dichloroacetate for 9.7 to 16.5 years: 8 patients, stable labs, nerve conduction changes (not DADA)

Clinical trial

Abdelmalak M et al. Mol Genet Metab. 2013;109(2):139-43. PMID 23611579.

8 patients with pyruvate dehydrogenase complex or respiratory chain deficiencies received oral dichloroacetate for 9.7 to 16.5 years. Hematological, electrolyte, renal and hepatic status remained stable and blood lactate stayed normal. Nerve conduction either did not change or decreased modestly, leading to dose reduction or temporary discontinuation in 3 of the 8, although symptomatic worsening of peripheral neuropathy did not occur.

Participants / model
8 patients with congenital causes of lactic acidosis
Treatment
Oral dichloroacetate for 9.7 to 16.5 years (dose not reproduced on this page)
Follow-up
9.7 to 16.5 years
Study design
Long-term open-label safety study
Funding
not stated in the source

Dosing here was set by weight in a monitored metabolic clinic, which is not how a supplement is taken. This is dichloroacetate, not DADA.

Read the original source
Dichloroacetate in congenital lactic acidosis: 43 children, no clinical benefit (not DADA)

Randomized controlled trial

Stacpoole PW et al. Pediatrics. 2006;117(5):1519-31. PMID 16651305.

A double-blind randomized controlled trial in 43 children aged 0.9 to 19 years with congenital lactic acidosis gave oral dichloroacetate or placebo for 6 months after a 6-month placebo preconditioning period. There were no significant differences in global assessment of treatment efficacy scores, linear growth, or frequency or severity of intercurrent illnesses. Dichloroacetate significantly decreased the rise in blood lactate after carbohydrate feeding. Chronic administration was associated with a fall in plasma clearance of the drug and a rise in urinary maleylacetone and delta-aminolevulinate.

Participants / model
43 children with congenital lactic acidosis
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
6 months after a 6-month placebo preconditioning period
Study design
Randomized double-blind placebo-controlled trial
Funding
not stated in the source

This is dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
FDA 503A proposed rule, 5 September 2019: sodium dichloroacetate not proposed for the bulks list

Regulatory record

U.S. Food and Drug Administration. Amendments to the List of Bulk Drug Substances That Can Be Used To Compound Drug Products in Accordance With Section 503A of the Federal Food, Drug, and Cosmetic Act. Proposed rule, Federal Register, 5 September 2019, 84 FR 46688. Current 21 CFR 216.23 read for the 1 October 2026 eCFR edition.

In a proposed rule published on 5 September 2019 (84 FR 46688), FDA evaluated sodium dichloroacetate for the section 503A compounding bulks list and proposed not to include it, stating significant safety concerns primarily related to its toxicity profile in nonclinical and clinical studies, that one identified study was closed due to patient deaths and safety concerns, that there is no evidence it would be effective in preventing or treating cancer, and that no evidence of historical use in compounded drug products was found. The Pharmacy Compounding Advisory Committee voted not to include it at its 23 June 2016 meeting. The current eCFR text of 21 CFR 216.23, read for the 1 October 2026 edition, lists sodium dichloroacetate neither among the substances that can be used nor among those formally determined not to be included, so the 2019 proposal has not been codified. No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and a DailyMed search for dichloroacetate on 9 October 2026 returned no labels.

Participants / model
FDA compounding evaluation, not a clinical population
Treatment
Bulk drug substance
Follow-up
Proposed rule of 5 September 2019; eCFR read for the 1 October 2026 edition
Study design
Federal Register proposed rule and current codified text
Funding
not stated in the source

The rule concerns sodium dichloroacetate, the anion's usual salt, not DADA. It is a proposal and has not been codified.

Read the original source
DADA in fatty liver: 127 enrolled, 123 analyzed, two doses, no placebo arm

Clinical trial

Lu LG et al. Zhonghua Gan Zang Bing Za Zhi. 2005;13(2):92-5. PMID 15727691.

A randomized double-blind dose-parallel trial in China enrolled 127 patients with nonalcoholic fatty liver disease, randomized to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, with 123 analyzed after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%).

Participants / model
127 enrolled, 123 analyzed, patients with nonalcoholic fatty liver disease
Treatment
Oral diisopropylamine dichloroacetate at two daily dose levels for 8 weeks (doses not reproduced on this page)
Follow-up
8 weeks
Study design
Randomized double-blind dose-comparison trial with no placebo arm
Funding
not stated in the source

The only controlled human trial of DADA itself located. There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

Read the original source

Why does DADA sit in D tier?

D because the compound and its evidence have come apart. Dichloroacetate has a long clinical record that is mostly small or null on clinical endpoints, while DADA has one two-dose trial without a placebo arm, a mutagenic Ames result for the salt and its amine, and a mouse study with supplier ties.

Dichloroacetate itself has a long, serious clinical record: a 252-patient randomized trial in lactic acidosis that lowered lactate and changed nothing that mattered, a 43-child randomized trial that missed its clinical endpoints, a 2026 phase 3 in 34 children that missed its primary endpoint and showed an effect only in the open-label extension, and a randomized MELAS trial stopped early because 17 of 19 patients discontinued for peripheral neuropathy. FDA proposed to keep its sodium salt off the 503A compounding list.

DADA is a different thing: the same anion attached to diisopropylamine, with one controlled human trial located anywhere, an 8-week two-dose comparison in 123 Chinese patients with fatty liver and no placebo arm. Beside it sit an Ames test in which both the salt and the amine were mutagenic, a mouse influenza model with supplier ties, and a name, pangamic acid, that has been attached to different chemicals in commercial products.

The supplier's phrase complicated history is accurate and is also the whole story. Nothing has been studied for the salt in healthy people, for performance, for body composition or by any injected route, and the peripheral neuropathy that ended a dichloroacetate trial is a dichloroacetate finding that no source ties to DADA.

Sodium dichloroacetate in lactic acidosis: 252 adults, lactate fell, survival did not change (not DADA)

Randomized controlled trial

Stacpoole PW et al. N Engl J Med. 1992;327(22):1564-9. PMID 1435883.

The Dichloroacetate-Lactic Acidosis Study Group randomized 252 adults with lactic acidosis (blood lactate at least 5.0 mmol/L with pH at most 7.35 or a base deficit of at least 6 mmol/L) to intravenous sodium dichloroacetate or placebo, 126 each. Lactate fell by 20% or more in 66% on dichloroacetate versus 36% on placebo (P = 0.001) and arterial pH rose more (P = 0.005), but the absolute differences were small and there was no improvement in hemodynamics or survival: 12% of dichloroacetate patients and 17% of placebo patients survived to hospital discharge. The authors call the changes statistically significant but clinically unimportant.

Participants / model
252 critically ill adults with lactic acidosis
Treatment
Intravenous sodium dichloroacetate or placebo
Follow-up
not stated in the source
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

This is sodium dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Dichloroacetate in congenital lactic acidosis: 43 children, no clinical benefit (not DADA)

Randomized controlled trial

Stacpoole PW et al. Pediatrics. 2006;117(5):1519-31. PMID 16651305.

A double-blind randomized controlled trial in 43 children aged 0.9 to 19 years with congenital lactic acidosis gave oral dichloroacetate or placebo for 6 months after a 6-month placebo preconditioning period. There were no significant differences in global assessment of treatment efficacy scores, linear growth, or frequency or severity of intercurrent illnesses. Dichloroacetate significantly decreased the rise in blood lactate after carbohydrate feeding. Chronic administration was associated with a fall in plasma clearance of the drug and a rise in urinary maleylacetone and delta-aminolevulinate.

Participants / model
43 children with congenital lactic acidosis
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
6 months after a 6-month placebo preconditioning period
Study design
Randomized double-blind placebo-controlled trial
Funding
not stated in the source

This is dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Sodium dichloroacetate phase 3, 2026: 34 children, primary endpoint missed (not DADA)

Randomized controlled trial

Stacpoole PW et al. JCI Insight. 2026;11(18). PMID 42770298.

A 2026 phase III multicenter trial in 34 children with pyruvate dehydrogenase complex deficiency randomized participants to 4 months of sodium dichloroacetate or placebo, then a 1-month washout and crossover, with an optional open-label extension, dosing set by GSTZ1 pharmacogenomic haplotype. The primary endpoint, the observer-reported outcomes motor domain score, was not significantly different between treatment and placebo (P = 0.512). Longer-term treatment including the open-label extension showed a significant treatment effect (P = 0.002), strongest in participants with higher baseline motor impairment (P = 0.001). Plasma lactate fell 0.48 (SD 0.82) mmol/L, 20%, P = 0.006, and survival exceeded a natural history cohort (log-rank P = 0.027). Chronic dosing was described as well tolerated and safe.

Participants / model
34 children with pyruvate dehydrogenase complex deficiency
Treatment
Oral sodium dichloroacetate, dose set by GSTZ1 haplotype, or placebo
Follow-up
4 months, 1-month washout and crossover, optional open-label extension
Study design
Randomized double-blind phase 3 trial with crossover and open-label extension
Funding
Several authors have financial interests in the sponsor or the study drug.

This is sodium dichloroacetate, not DADA. The primary endpoint was missed, and the effect appeared only with longer treatment including the open-label extension.

Read the original source
Dichloroacetate in MELAS: 30 patients, stopped early for peripheral neuropathy (not DADA)

Randomized controlled trial

Kaufmann P et al. Neurology. 2006;66(3):324-30. PMID 16476929.

A double-blind placebo-controlled randomized 3-year crossover trial of dichloroacetate in 30 patients aged 10 to 60 with MELAS and the A3243G mutation was terminated early for peripheral nerve toxicity. During the initial 24-month treatment period, 15 of 15 patients randomized to dichloroacetate were taken off study medication versus 4 of 15 on placebo, and study medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. The mean global assessment score did not differ between arms.

Participants / model
30 patients aged 10 to 60 with MELAS
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
Planned 3 years; terminated early
Study design
Randomized double-blind placebo-controlled crossover trial
Funding
not stated in the source

Peripheral neuropathy is a dichloroacetate finding with this trial attached. No source ties it to DADA.

Read the original source
DADA in fatty liver: 127 enrolled, 123 analyzed, two doses, no placebo arm

Clinical trial

Lu LG et al. Zhonghua Gan Zang Bing Za Zhi. 2005;13(2):92-5. PMID 15727691.

A randomized double-blind dose-parallel trial in China enrolled 127 patients with nonalcoholic fatty liver disease, randomized to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, with 123 analyzed after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%).

Participants / model
127 enrolled, 123 analyzed, patients with nonalcoholic fatty liver disease
Treatment
Oral diisopropylamine dichloroacetate at two daily dose levels for 8 weeks (doses not reproduced on this page)
Follow-up
8 weeks
Study design
Randomized double-blind dose-comparison trial with no placebo arm
Funding
not stated in the source

The only controlled human trial of DADA itself located. There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

Read the original source
Ames test: both DADA and diisopropylamine alone were mutagenic

Cell study

Gelernt MD et al. Nutr Cancer. 1982;3(3):129-33. PMID 6752894.

In the Ames Salmonella mammalian microsome mutagenicity test, both diisopropylamine dichloroacetate and diisopropylamine alone demonstrated mutagenicity. The authors note that 90% of such agents prove carcinogenic and that this must be considered in any proposed use of pangamic acid containing either substance.

Participants / model
Salmonella strains with mammalian microsomal activation
Treatment
In vitro exposure
Follow-up
Not applicable
Study design
Original in vitro toxicology study
Funding
not stated in the source

This is a bacterial assay, not a human finding, and no human carcinogenicity data were located.

Read the original source
Mouse influenza model: oral DADA restored PDH activity and ATP; supplier ties

Animal study

Yamane K et al. PLoS One. 2014;9(5):e98032. PMID 24865588.

Mice infected with influenza A PR/8/34 (H1N1) showed down-regulated pyruvate dehydrogenase activity and ATP, with up-regulated PDK4 in skeletal muscle, heart, liver and lungs. Oral DADA at 12-hour intervals for 14 days restored PDH activity and ATP, improved glucose and lipid metabolism, improved survival, and suppressed cytokine responses and viral replication. DADA is characterized here as a PDK4 inhibitor.

Participants / model
Mice infected with influenza A H1N1
Treatment
Oral DADA every 12 hours for 14 days; dose not stated in the source
Follow-up
14 days
Study design
Original animal infection study
Funding
Two authors were employed by the company that supplied the compound, and five are inventors on a patent application covering it for influenza.

This is a mouse infection model and supports no human claim.

Read the original source
1999 analytical study: pangamic acid products held gluconic acid, glycine or DADA

Chemical identity record

Schneider D et al. Arzneimittelforschung. 1999;49(4):335-43. PMID 10337453.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate. The authors also report that high concentrations of DIPA deteriorated mitochondrial respiratory control in vitro by increasing state IV oxygen consumption.

Participants / model
Commercial products and isolated mitochondria
Treatment
Marketed oral products; in vitro exposure
Follow-up
Not applicable
Study design
Original analytical and mechanistic study
Funding
not stated in the source

A product label saying pangamic acid or vitamin B15 does not identify the molecule inside. The mitochondrial result is in vitro.

Read the original source
PubMed search, 9 October 2026: 10 records, none on performance, body composition or injection

PubMed search record

PubMed search run on 9 October 2026: (diisopropylamine dichloroacetate OR diisopropylammonium dichloroacetate) AND (exercise OR performance OR athletes OR bodybuilding OR injection OR injectable OR intramuscular OR subcutaneous). 10 records returned.

The search returned 10 records. None studied DADA in humans for performance, body composition or any injected route. They covered poultry liver morphology, insect gene editing, a doping-control assay for diisopropylamine in horse urine, two mouse tumor xenograft studies, a rat steatohepatitis herbal study, a postoperative pain scale, a rat teratology study of an unrelated compound, a cholinesterase enzymology paper, and a 1963 report of intracarotid injection in vascular patients. No human efficacy, pharmacokinetic or safety data exist for any injected DADA preparation in the records reviewed.

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

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

Read the original source

Studies and sources

PubChem: DADA identity and how it differs from sodium dichloroacetate

Chemical identity record

National Library of Medicine. PubChem compound records CID 12617 (diisopropylammonium dichloroacetate), CID 6597 (dichloroacetic acid) and CID 517326 (sodium dichloroacetate).

DADA, diisopropylammonium dichloroacetate: PubChem CID 12617, C8H17Cl2NO2, molecular weight 230.13 g/mol, CAS 660-27-5; listed synonyms include diisopropylamine dichloroacetate, Dipromonium, Kalodil, Oxypangam and IS-401. It is a salt of dichloroacetic acid with diisopropylamine, so it dissociates into two moieties. Dichloroacetic acid itself is CID 6597, C2H2Cl2O2, 128.94 g/mol, CAS 79-43-6. The salt used in nearly all of the clinical dichloroacetate research is sodium dichloroacetate, CID 517326, C2HCl2NaO2, 150.92 g/mol, CAS 2156-56-1. DADA and sodium dichloroacetate share an anion and nothing else, and the diisopropylamine half has its own pharmacology.

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

Identity record only. The distinction between DADA and sodium dichloroacetate is the point of the record: findings for one are not findings for the other.

Read the original source
1999 analytical study: pangamic acid products held gluconic acid, glycine or DADA

Chemical identity record

Schneider D et al. Arzneimittelforschung. 1999;49(4):335-43. PMID 10337453.

A 1999 analytical study reports that pangamic acid, described in 1938 as 6-O-(dimethylaminoacetyl)-D-gluconic acid, has been marketed for decades, and that diisopropylammonium dichloroacetate, a synthetic product not found in biological material, is also marketed claiming similar functions. Chemical identification of commercially available German market products declared as pangamic acid found three separate substances across them: gluconic acid, glycine and diisopropylammonium dichloroacetate. The authors also report that high concentrations of DIPA deteriorated mitochondrial respiratory control in vitro by increasing state IV oxygen consumption.

Participants / model
Commercial products and isolated mitochondria
Treatment
Marketed oral products; in vitro exposure
Follow-up
Not applicable
Study design
Original analytical and mechanistic study
Funding
not stated in the source

A product label saying pangamic acid or vitamin B15 does not identify the molecule inside. The mitochondrial result is in vitro.

Read the original source
Pangamic acid trial: 16 male track athletes, null result, product did not contain DADA

Clinical trial

Gray ME et al. Med Sci Sports Exerc. 1982;14(6):424-7. PMID 7162387.

In a double-blind study, 16 male track athletes took pangamic acid tablets, stated in the paper as calcium gluconate and N,N-dimethylglycine, or placebo for three weeks and were tested on the Bruce treadmill protocol. MANOVA found no significant differences between groups after treatment in maximal heart rate, treadmill time, recovery heart rate, or post-test blood glucose and lactate.

Participants / model
16 male track athletes
Treatment
Oral tablets of calcium gluconate plus dimethylglycine, or placebo (dose not reproduced on this page)
Follow-up
3 weeks
Study design
Double-blind placebo-controlled study
Funding
not stated in the source

The one controlled human performance study carried out under the pangamic acid name tested a different chemical entirely. It is a null result for a product that did not contain DADA.

Read the original source
Sodium dichloroacetate in lactic acidosis: 252 adults, lactate fell, survival did not change (not DADA)

Randomized controlled trial

Stacpoole PW et al. N Engl J Med. 1992;327(22):1564-9. PMID 1435883.

The Dichloroacetate-Lactic Acidosis Study Group randomized 252 adults with lactic acidosis (blood lactate at least 5.0 mmol/L with pH at most 7.35 or a base deficit of at least 6 mmol/L) to intravenous sodium dichloroacetate or placebo, 126 each. Lactate fell by 20% or more in 66% on dichloroacetate versus 36% on placebo (P = 0.001) and arterial pH rose more (P = 0.005), but the absolute differences were small and there was no improvement in hemodynamics or survival: 12% of dichloroacetate patients and 17% of placebo patients survived to hospital discharge. The authors call the changes statistically significant but clinically unimportant.

Participants / model
252 critically ill adults with lactic acidosis
Treatment
Intravenous sodium dichloroacetate or placebo
Follow-up
not stated in the source
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

This is sodium dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Dichloroacetate in MELAS: 30 patients, stopped early for peripheral neuropathy (not DADA)

Randomized controlled trial

Kaufmann P et al. Neurology. 2006;66(3):324-30. PMID 16476929.

A double-blind placebo-controlled randomized 3-year crossover trial of dichloroacetate in 30 patients aged 10 to 60 with MELAS and the A3243G mutation was terminated early for peripheral nerve toxicity. During the initial 24-month treatment period, 15 of 15 patients randomized to dichloroacetate were taken off study medication versus 4 of 15 on placebo, and study medication was discontinued in 17 of 19 patients because of onset or worsening of peripheral neuropathy. The mean global assessment score did not differ between arms.

Participants / model
30 patients aged 10 to 60 with MELAS
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
Planned 3 years; terminated early
Study design
Randomized double-blind placebo-controlled crossover trial
Funding
not stated in the source

Peripheral neuropathy is a dichloroacetate finding with this trial attached. No source ties it to DADA.

Read the original source
Dichloroacetate in congenital lactic acidosis: 43 children, no clinical benefit (not DADA)

Randomized controlled trial

Stacpoole PW et al. Pediatrics. 2006;117(5):1519-31. PMID 16651305.

A double-blind randomized controlled trial in 43 children aged 0.9 to 19 years with congenital lactic acidosis gave oral dichloroacetate or placebo for 6 months after a 6-month placebo preconditioning period. There were no significant differences in global assessment of treatment efficacy scores, linear growth, or frequency or severity of intercurrent illnesses. Dichloroacetate significantly decreased the rise in blood lactate after carbohydrate feeding. Chronic administration was associated with a fall in plasma clearance of the drug and a rise in urinary maleylacetone and delta-aminolevulinate.

Participants / model
43 children with congenital lactic acidosis
Treatment
Oral dichloroacetate or placebo (dose not reproduced on this page)
Follow-up
6 months after a 6-month placebo preconditioning period
Study design
Randomized double-blind placebo-controlled trial
Funding
not stated in the source

This is dichloroacetate, not DADA. No result here applies to DADA.

Read the original source
Sodium dichloroacetate phase 3, 2026: 34 children, primary endpoint missed (not DADA)

Randomized controlled trial

Stacpoole PW et al. JCI Insight. 2026;11(18). PMID 42770298.

A 2026 phase III multicenter trial in 34 children with pyruvate dehydrogenase complex deficiency randomized participants to 4 months of sodium dichloroacetate or placebo, then a 1-month washout and crossover, with an optional open-label extension, dosing set by GSTZ1 pharmacogenomic haplotype. The primary endpoint, the observer-reported outcomes motor domain score, was not significantly different between treatment and placebo (P = 0.512). Longer-term treatment including the open-label extension showed a significant treatment effect (P = 0.002), strongest in participants with higher baseline motor impairment (P = 0.001). Plasma lactate fell 0.48 (SD 0.82) mmol/L, 20%, P = 0.006, and survival exceeded a natural history cohort (log-rank P = 0.027). Chronic dosing was described as well tolerated and safe.

Participants / model
34 children with pyruvate dehydrogenase complex deficiency
Treatment
Oral sodium dichloroacetate, dose set by GSTZ1 haplotype, or placebo
Follow-up
4 months, 1-month washout and crossover, optional open-label extension
Study design
Randomized double-blind phase 3 trial with crossover and open-label extension
Funding
Several authors have financial interests in the sponsor or the study drug.

This is sodium dichloroacetate, not DADA. The primary endpoint was missed, and the effect appeared only with longer treatment including the open-label extension.

Read the original source
Dichloroacetate for 9.7 to 16.5 years: 8 patients, stable labs, nerve conduction changes (not DADA)

Clinical trial

Abdelmalak M et al. Mol Genet Metab. 2013;109(2):139-43. PMID 23611579.

8 patients with pyruvate dehydrogenase complex or respiratory chain deficiencies received oral dichloroacetate for 9.7 to 16.5 years. Hematological, electrolyte, renal and hepatic status remained stable and blood lactate stayed normal. Nerve conduction either did not change or decreased modestly, leading to dose reduction or temporary discontinuation in 3 of the 8, although symptomatic worsening of peripheral neuropathy did not occur.

Participants / model
8 patients with congenital causes of lactic acidosis
Treatment
Oral dichloroacetate for 9.7 to 16.5 years (dose not reproduced on this page)
Follow-up
9.7 to 16.5 years
Study design
Long-term open-label safety study
Funding
not stated in the source

Dosing here was set by weight in a monitored metabolic clinic, which is not how a supplement is taken. This is dichloroacetate, not DADA.

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FDA 503A proposed rule, 5 September 2019: sodium dichloroacetate not proposed for the bulks list

Regulatory record

U.S. Food and Drug Administration. Amendments to the List of Bulk Drug Substances That Can Be Used To Compound Drug Products in Accordance With Section 503A of the Federal Food, Drug, and Cosmetic Act. Proposed rule, Federal Register, 5 September 2019, 84 FR 46688. Current 21 CFR 216.23 read for the 1 October 2026 eCFR edition.

In a proposed rule published on 5 September 2019 (84 FR 46688), FDA evaluated sodium dichloroacetate for the section 503A compounding bulks list and proposed not to include it, stating significant safety concerns primarily related to its toxicity profile in nonclinical and clinical studies, that one identified study was closed due to patient deaths and safety concerns, that there is no evidence it would be effective in preventing or treating cancer, and that no evidence of historical use in compounded drug products was found. The Pharmacy Compounding Advisory Committee voted not to include it at its 23 June 2016 meeting. The current eCFR text of 21 CFR 216.23, read for the 1 October 2026 edition, lists sodium dichloroacetate neither among the substances that can be used nor among those formally determined not to be included, so the 2019 proposal has not been codified. No dichloroacetate salt appears in Drugs@FDA as an approved active ingredient, and a DailyMed search for dichloroacetate on 9 October 2026 returned no labels.

Participants / model
FDA compounding evaluation, not a clinical population
Treatment
Bulk drug substance
Follow-up
Proposed rule of 5 September 2019; eCFR read for the 1 October 2026 edition
Study design
Federal Register proposed rule and current codified text
Funding
not stated in the source

The rule concerns sodium dichloroacetate, the anion's usual salt, not DADA. It is a proposal and has not been codified.

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DADA in fatty liver: 127 enrolled, 123 analyzed, two doses, no placebo arm

Clinical trial

Lu LG et al. Zhonghua Gan Zang Bing Za Zhi. 2005;13(2):92-5. PMID 15727691.

A randomized double-blind dose-parallel trial in China enrolled 127 patients with nonalcoholic fatty liver disease, randomized to diisopropylamine dichloroacetate at one of two daily dose levels for 8 weeks, with 123 analyzed after 4 exclusions and no dropouts. Overall improvement in clinical symptoms was 87.8% and 79.6% in the higher-dose and lower-dose groups, ALT normalization 55.7% and 69.4%, serum lipids lowered in 67.2% and 67.7%, and ultrasound grading improved in 51.7% and 43.5%, with no statistically significant differences between the two doses. One patient in each group reported dry mouth (1.6%).

Participants / model
127 enrolled, 123 analyzed, patients with nonalcoholic fatty liver disease
Treatment
Oral diisopropylamine dichloroacetate at two daily dose levels for 8 weeks (doses not reproduced on this page)
Follow-up
8 weeks
Study design
Randomized double-blind dose-comparison trial with no placebo arm
Funding
not stated in the source

The only controlled human trial of DADA itself located. There was no placebo arm, so the trial compares two doses of the same drug and cannot establish efficacy against no treatment.

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Ames test: both DADA and diisopropylamine alone were mutagenic

Cell study

Gelernt MD et al. Nutr Cancer. 1982;3(3):129-33. PMID 6752894.

In the Ames Salmonella mammalian microsome mutagenicity test, both diisopropylamine dichloroacetate and diisopropylamine alone demonstrated mutagenicity. The authors note that 90% of such agents prove carcinogenic and that this must be considered in any proposed use of pangamic acid containing either substance.

Participants / model
Salmonella strains with mammalian microsomal activation
Treatment
In vitro exposure
Follow-up
Not applicable
Study design
Original in vitro toxicology study
Funding
not stated in the source

This is a bacterial assay, not a human finding, and no human carcinogenicity data were located.

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Mouse influenza model: oral DADA restored PDH activity and ATP; supplier ties

Animal study

Yamane K et al. PLoS One. 2014;9(5):e98032. PMID 24865588.

Mice infected with influenza A PR/8/34 (H1N1) showed down-regulated pyruvate dehydrogenase activity and ATP, with up-regulated PDK4 in skeletal muscle, heart, liver and lungs. Oral DADA at 12-hour intervals for 14 days restored PDH activity and ATP, improved glucose and lipid metabolism, improved survival, and suppressed cytokine responses and viral replication. DADA is characterized here as a PDK4 inhibitor.

Participants / model
Mice infected with influenza A H1N1
Treatment
Oral DADA every 12 hours for 14 days; dose not stated in the source
Follow-up
14 days
Study design
Original animal infection study
Funding
Two authors were employed by the company that supplied the compound, and five are inventors on a patent application covering it for influenza.

This is a mouse infection model and supports no human claim.

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Horse racing laboratory: diisopropylamine is a banned substance with a detection method

Chemical identity record

Kwak YB et al. J Pharm Biomed Anal. 2023;234:115576. PMID 37459832.

A horse racing laboratory paper states that diisopropylamine is used as an intravenous antihypertensive agent and is prohibited in the horse racing industry because of performance enhancing effects, and reports identifying an N-oxidized metabolite of DIPA, produced mainly by flavin-containing monooxygenase, in an actual horse urine sample that tested positive for DIPA.

Participants / model
Horse urine samples and in vitro liver preparations
Treatment
Not stated for the positive sample; in vitro for the metabolism work
Follow-up
Not applicable
Study design
Original analytical study for doping control
Funding
not stated in the source

This establishes that the diisopropylamine half is a banned substance in equine racing with a detection method behind it. It is not a human performance result, and the paper reports none.

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Why is DADA in D tier?

D fits a compound whose evidence has come apart from its name. Dichloroacetate has a long clinical record, but DADA has one two-dose trial with no placebo arm, a mutagenic Ames result for the salt and its amine, and a mouse study with supplier ties. The dichloroacetate results belong to a different salt and do not transfer.