This page is a review of published research. It is not an offer of treatment and does not describe a service. It exists because patients ask about these compounds, and because the information available online is unusually poor in both directions — pages that promise a great deal, and pages that dismiss the underlying science without describing it.

Neither compound is approved by the FDA for intravenous use, in any condition. Nothing here is medical advice or a recommendation to use, obtain, or avoid either substance. Discuss any therapy with your treating physician, particularly if you are undergoing cancer treatment.

Dichloroacetate (DCA)

The idea behind it is real science

The interest in DCA is not folklore. It comes from a genuine and well-published observation about how tumor cells make energy. Most cancer cells favor glycolysis over mitochondrial oxidation even when oxygen is plentiful, a pattern described by Otto Warburg in the 1920s. One consequence is that the mitochondria in those cells stay relatively quiet, and quiet mitochondria are less likely to trigger apoptosis, the cell’s built-in self-destruct program.

DCA inhibits pyruvate dehydrogenase kinase. Blocking that enzyme pushes pyruvate back into the mitochondria and restarts oxidative metabolism. In 2007, a University of Alberta group led by Evangelos Michelakis published in Cancer Cell that doing this in cancer cell lines and rodent tumors reactivated mitochondrial function, restored a potassium-channel signal, and induced apoptosis in cancer cells while largely sparing normal ones. [1]

That paper is legitimate, widely cited, and the reason DCA has held attention for two decades. It is also, importantly, a laboratory paper. It enrolled no patients. Michelakis said so himself in a 2008 review: “No patient with cancer has received DCA within a clinical trial.” [2]

How DCA has actually been given

This is the detail most often lost in translation. Across every registered oncology trial, DCA has been given orally, not intravenously — typically 6.25 to 25 mg/kg twice daily, taken by mouth. The upper end of that range was not sustainable; trials repeatedly had to reduce it.

Intravenous DCA has never been studied in a human cancer trial. It is not an unproven version of a proven therapy — it is unstudied.

What happened when it reached patients

Study	Patients	Design	Result
Michelakis 2010 Glioblastoma, Alberta	5 treated	Open-label, no control group, patients also on standard treatment	Authors’ wording: “indications of clinical efficacy were present.” Dose-limiting reversible peripheral neuropathy at higher doses forced a reduction to 6.25 mg/kg twice daily.
Dunbar 2013 Recurrent glioma	15	Phase I, dose-finding	No objective tumor responses.
Chu 2015 Advanced solid tumors, Canada	24	Phase I, single-arm	“No responses were observed and eight patients had stable disease.” Three of seven patients at the next dose up had dose-limiting fatigue, vomiting and diarrhea.
Garon 2014 Lung and breast cancer	7	Phase II — terminated early	“Patients with previously treated advanced NSCLC did not benefit from oral DCA.” Two patients died within a week of starting; causality judged uncertain, but the trial did not continue.
Powell 2022 Head and neck cancer	45	Randomized, double-blind, placebo-controlled	Complete response at end of treatment was higher with DCA (71.4% vs 37.5%), but five-year progression-free and overall survival were no different. More fevers (43% vs 8%) and thrombocytopenia (67% vs 33%).

The Powell trial is the only randomized placebo-controlled study of DCA in oncology, and therefore the most informative single study on this page. Its primary endpoint was safety, not efficacy.

A 2024 independent scoping review pooled everything published on DCA in cancer patients: twelve studies, sixty-five patients in total, between 2010 and 2019. Its conclusion was that “there is insufficient evidence to affirm that treatment with DCA in cancer patients is effective or is safe.” [15]

The safety finding that is actually reproducible

The most consistent human result for DCA is not an efficacy result. It is peripheral neuropathy — numbness, tingling and nerve conduction changes in the hands and feet — and it is dose-dependent.

The clearest demonstration came from outside oncology. A randomized, placebo-controlled trial of DCA in MELAS, a mitochondrial disease, was halted early because 17 of 19 patients had to stop the drug for new or worsening neuropathy. In the first 24 months, all 15 patients on DCA discontinued, compared with 4 on placebo. [12] A separate long-term study in children with congenital lactic acidosis, followed over 110 patient-years, found measurable slowing of peroneal nerve conduction. [11]

At trial doses the neuropathy is generally reversible when the drug is stopped. Two things make it hard to predict in an individual: it tracks with blood levels rather than with the milligram dose, and blood levels depend heavily on GSTZ1 genotype. Two people at the same mg/kg dose can have very different exposures, and the person who accumulates the drug is the person who gets hurt. An Australian myeloma pilot observed exactly this — the patient with the highest exposure had the strongest neuropathy. [8]

There is also a documented death. A 52-year-old man with glioblastoma received an unknown quantity of DCA from an alternative practitioner together with intravenous artesunate, developed liver injury and bone marrow suppression within days, and died ten days after the infusion. The causality assessment found a reasonable probability that the combination caused the liver injury. [13] A separate case report describes severe encephalopathy — confusion, unsteady gait, slurred speech — in a melanoma patient self-administering capsules labeled DCA. [14]

Dimethyl sulfoxide (DMSO)

What DMSO is genuinely approved for

DMSO has one FDA-approved medical indication, and the evidence behind it is real. Marketed as Rimso-50, a 50% solution instilled directly into the bladder through a catheter, it is approved for symptomatic relief of interstitial cystitis. A randomized placebo-controlled crossover trial found 53% versus 18% markedly improved by subjective measures, [10] and a 2025 meta-analysis of 14 studies and 554 patients confirmed significant reductions in symptom scores and pain — alongside an adverse event rate of 37.6%. [16]

That is the whole of it. No intravenous or systemic DMSO product is approved as a drug anywhere in the world. Where DMSO appears inside an approved injectable product, it is functioning as a solvent carrying the actual active ingredient, not as the therapy.

The systemic human record

Searching for controlled trials of intravenous DMSO turns up very little, and what exists is old and small. The strongest case — and it is not strong — is a group of three uncontrolled series in severe head injury, published between 1984 and 1991, enrolling six to ten patients each. None was randomized. None has been replicated in the thirty-five years since.

The lead author of the first of these, writing about his own results, concluded that DMSO was “extremely complex to use, and difficulties with its administration may make its risks ultimately greater than its potential benefits.” [17] That is a fair summary of the systemic DMSO literature as a whole.

Study	Patients	Design	Result
Williams 1985 Scleroderma digital ulcers	84	Double-blind multicenter randomized trial, topical	“There were no statistically significant differences among the 3 treatment groups” on any endpoint. More than a quarter of the 70% group withdrew for skin toxicity.
Amemori 2006 Amyloidosis, Japan	15	Retrospective chart review, oral 3–20 g/day	Ten of fifteen classified as successfully treated. No control group — the weakest design that still counts as clinical evidence.
Burke 2022 Basal cell carcinoma	25 patients, 29 lesions	Randomized, topical	Topical 30% ascorbic acid in 95% DMSO versus imiquimod: 86.7% vs 57.1% clearance at 8 weeks, converging to non-inferiority by 12 weeks, high-risk sites excluded.

The Burke study is worth flagging clearly, because it is the source of the “86% cure rate” figure circulating on social media as evidence that DMSO treats cancer. It is a 25-patient study of a cream applied to skin lesions. It says nothing about intravenous DMSO or about internal cancers.

A note on the two oral cancer trials you may find

Two published trials report a survival benefit from oral DMSO in gastric and colonic cancer. Both are single-author papers by the same investigator. In 1994, the executive editorial committee of the Journal of Laboratory and Clinical Medicine published a formal notice titled “Allegations of impropriety in manuscripts by Aws S. Salim: examination and withdrawal of journal aegis.” [18] We could not confirm that these two specific oncology papers were retracted, but an author-level finding of that kind means the results cannot be treated as reliable. If you encounter them cited as proof that DMSO treats cancer, this is the missing context.

Systemic safety

Systemic DMSO is not inert, and the harms are documented rather than theoretical.

Hemolysis and enzyme elevation. The first report of intravenous DMSO in humans described two elderly patients with rises in AST, hydroxybutyrate dehydrogenase and CK, plus evidence of red blood cell destruction. One became seriously ill. [19]
Serious neurologic and cardiac events. The largest real-world experience with intravenous DMSO comes from stem cell transplantation, where it is infused as a cryoprotectant. That literature contains reports of seizure with cardiac arrest, encephalopathy, stroke, myocardial infarction and bilateral thalamic infarction. [20–23]
Intracerebral hemorrhage in a self-treating patient. A man in his seventies sustained two separate frontal lobe hemorrhages while self-treating with DMSO. The authors concluded DMSO was a likely causative agent. [24]
Eye findings. Lens opacities in three animal species halted DMSO’s clinical development in 1965 and are why the approved product’s label still requires slit-lamp examinations before and during treatment.
The odor. A garlic-like taste appears within minutes, and breath and skin odor persist up to 72 hours. It is unavoidable and dose-independent.

In Australia, the Federal Court restrained a supplier from advertising or supplying products containing DMSO in June 2020; DMSO is not on the Australian Register of Therapeutic Goods. [25]

What “overseas research” actually refers to

Both compounds are frequently described as being “used successfully overseas,” with the implication that a body of foreign evidence exists that Americans are not being told about. We went looking for it specifically. Here is the entirety of what that phrase points to.

Source	Country	Size	What it establishes
Michelakis, glioblastoma	Canada	5 patients	Hypothesis-generating only; no control group
Chu, solid tumors	Canada	24 patients	Dose ceiling; no objective responses
Tian, myeloma pilot	Australia	7 patients	Uncontrolled; neuropathy tracked with exposure
Karaca / Kulah, head injury	Turkey	10 each	Uncontrolled series, 1990–1991, never replicated
Amemori, amyloidosis	Japan	15 patients	Retrospective chart review, oral route
Perez, CRPS	Netherlands	146 patients	Topical; equivalent to another unproven agent, no placebo arm
Soviet-era scleroderma reports	USSR	Not stated	1983–1985; methodology not verifiable

Two observations. First, the largest and best-designed studies in this set — the Canadian phase I and the Dutch CRPS trial — are the ones that failed to show benefit. Second, the international literature is not being suppressed. It is indexed in PubMed, it is freely searchable, and the reason it is not more widely cited is that it is small, old and largely uncontrolled.

Where the research is actually going

The honest positive note is not in the existing cancer data. It is in metabolic disease, where DCA is closer to becoming an approved drug than most people following the cancer story realize.

Pyruvate dehydrogenase complex deficiency. Saol Therapeutics submitted a New Drug Application for sodium dichloroacetate in this rare inherited metabolic disorder. FDA issued a Complete Response Letter in September 2025; the application was resubmitted in July 2026 with a decision date of December 30, 2026. If approved, it would be the first approved DCA product — for a metabolic indication, not cancer.
Two ongoing glioblastoma trials. NCT05120284 (University of Florida, with Johns Hopkins and Wake Forest) and NCT05173623 (Sidney Kimmel) are both active. Note what the Florida trial is measuring: a pharmacodynamic marker of whether the drug is hitting its target, not tumor response. That is the appropriate next question after two phase I trials produced no objective responses.
An unresolved gap. A University of Alberta phase II trial in brain cancer (NCT00540176, 40 patients) is listed as completed in August 2009. Seventeen years later we could find no published results. That absence is itself worth knowing about.

If you are considering either one

People generally arrive at these compounds while dealing with something serious, often after conventional options have narrowed. That is a reasonable place to be, and it deserves better than either a sales pitch or a lecture. A few things we would want anyone to know before deciding.

Ask which route the evidence you were shown used. If someone cites the DCA cancer research to support an intravenous infusion, the citation does not support the offer — every one of those trials was oral.
Ask where the substance comes from. Neither compound has an FDA-approved injectable form, which means any IV preparation is compounded or sourced outside the regulated supply chain. Purity and concentration are not guaranteed, and both documented serious harms above involved material obtained outside a clinical trial.
Tell your oncologist. Not for permission — for safety. DCA’s neuropathy is additive with the neuropathy caused by platinum agents and taxanes, and the one fatal case involved a drug combination.
Do not substitute. The clearest documented harm from unproven cancer therapies is not usually the therapy itself. It is delay of treatment that works.
Consider a trial. If the mechanism interests you, the two active glioblastoma studies are enrolling under protocols with monitoring, known dosing, and no cost for the investigational agent.

Citations

Every reference below was verified against PubMed or a primary registry.

Bonnet S, Archer SL, Allalunis-Turner J, et al. A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer Cell 2007;11(1):37–51. PMID 17222789
Michelakis ED, Webster L, Mackey JR. Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Br J Cancer 2008;99:989–994. PMID 18766181
Michelakis ED, Sutendra G, Dromparis P, et al. Metabolic modulation of glioblastoma with dichloroacetate. Sci Transl Med 2010;2(31):31ra34. PMID 20463368
Dunbar EM, Coats BS, Shroads AL, et al. Phase 1 trial of dichloroacetate in patients with recurrent malignant brain tumors. Invest New Drugs 2014;32:452–464. PMID 24297161
Chu QS, Sangha R, Spratlin J, et al. A phase I open-labeled, single-arm, dose-escalation study of dichloroacetate in patients with advanced solid tumors. Invest New Drugs 2015;33:603–610. PMID 25762000
Garon EB, Christofk HR, Hosmer W, et al. Dichloroacetate should be considered with platinum-based chemotherapy in hypoxic tumors rather than as a single agent in advanced non-small cell lung cancer. J Cancer Res Clin Oncol 2014;140:443–452. PMID 24442098 · NCT01029925
Powell SF, Mazurczak M, Dib EG, et al. Phase II study of dichloroacetate, an inhibitor of pyruvate dehydrogenase, in combination with chemoradiotherapy for unresected, locally advanced head and neck squamous cell carcinoma. Invest New Drugs 2022;40:622–633. PMID 35312941 · NCT01386632
Tian DD, Bennett SK, Coupland LA, et al. GSTZ1 genotypes correlate with dichloroacetate pharmacokinetics and chronic side effects in multiple myeloma patients. Pharmacol Res Perspect 2019;7(6):e00526. PMID 31624634
Stacpoole PW, Kerr DS, Barnes C, et al. Controlled clinical trial of dichloroacetate for treatment of congenital lactic acidosis in children. Pediatrics 2006;117(5):1519–1531. PMID 16651305
Perez-Marrero R, Emerson LE, Feltis JT. A controlled study of dimethyl sulfoxide in interstitial cystitis. J Urol 1988;140(1):36–39. PMID 3288775
Stacpoole PW, Gilbert LR, Neiberger RE, et al. Evaluation of long-term treatment of children with congenital lactic acidosis with dichloroacetate. Pediatrics 2008;121(5):e1223–e1228. PMID 18411236
Kaufmann P, Engelstad K, Wei Y, et al. Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled clinical trial. Neurology 2006;66(3):324–330. PMID 16476929
Uhl M, Schwab S, Efferth T. Fatal liver and bone marrow toxicity by combination treatment of dichloroacetate and artesunate in a glioblastoma multiforme patient. Front Oncol 2016;6:204. PMID 27774434
Brandsma D, Dorlo TPC, Haanen JH, et al. Severe encephalopathy and polyneuropathy induced by dichloroacetate. J Neurol 2010;257(12):2099–2100. PMID 20632025
Bianchi C, Martinelli RP, Rozados VR, Scharovsky OG. Use of sodium dichloroacetate for cancer treatment: a scoping review. Medicina (B Aires) 2024;84(2):313–323. PMID 38683516
Li HR, et al. Efficacy and safety of intravesical dimethyl sulfoxide for interstitial cystitis/bladder pain syndrome. Neurourol Urodyn 2025;44(5):1036–1046. PMID 40205912
Marshall LF, Camp PE, Bowers SA. Dimethyl sulfoxide for the treatment of intracranial hypertension: a preliminary trial. Neurosurgery 1984;14(6):659–663. PMID 6462399
Hammerschmidt DE, Gross AG. Allegations of impropriety in manuscripts by Aws S. Salim: examination and withdrawal of journal aegis. J Lab Clin Med 1994;123(6):795–799. PMID 8201253
Yellowlees P, Greenfield C, McIntyre N. Dimethylsulphoxide-induced toxicity. Lancet 1980;2(8202):1004–1006. PMID 6107630
Maral S, et al. Dimethyl sulfoxide-induced tonic-clonic seizure and cardiac arrest during infusion of autologous peripheral blood stem cells. Cell Tissue Bank 2018;19(4):831–832. PMID 30099684
Chen-Plotkin AS, et al. Encephalopathy, stroke, and myocardial infarction with DMSO use in stem cell transplantation. Neurology 2007;68(11):859–861. PMID 17353475
Hentschke S, et al. Bilateral thalamic infarction after peripheral blood stem cell transplantation. Leuk Lymphoma 2006;47(11):2418–2420. PMID 17107921
González-López TJ, et al. Ischemic stroke associated with the infusion of DMSO-cryopreserved auto-PBSCs. Bone Marrow Transplant 2011;46(7):1035–1036. PMID 20956954
Olds J, et al. Recurrent intracerebral haemorrhage associated with dimethyl sulfoxide use. BMJ Case Rep 2021;14(2):e240371. PMID 33541956
Therapeutic Goods Administration. Federal Court restrains MMS Australia from advertising and supplying MMS and DMSO. 4 June 2020.
Williams HJ, et al. Double-blind multicenter controlled trial comparing topical dimethyl sulfoxide and normal saline for treatment of hand ulcers in scleroderma. Arthritis Rheum 1985;28(3):308–314. PMID 3884019
Amemori S, et al. Oral dimethyl sulfoxide for systemic amyloid A amyloidosis complicated with gastrointestinal symptoms. J Gastroenterol 2006;41(5):444–449. PMID 16799886
Burke B, Bailie JE. Randomized trial of topical ascorbic acid in DMSO versus imiquimod for the treatment of basal cell carcinoma. Biomed Pharmacother 2022;148:112710. PMID 35217280
Perez RSGM, et al. The treatment of complex regional pain syndrome type I with free radical scavengers: a randomized controlled study. Pain 2003;102(3):297–307. PMID 12670672
RIMSO-50 (dimethyl sulfoxide irrigation, USP 50% w/w) prescribing information. NDA 017788.

Alvin Philipose, DC, ICCP — Venturis Clinic, Oklahoma City and surrounding areas, including Tulsa. Last reviewed August 2026.

This page is for general education and reviews published research only. It is not medical advice, does not establish a doctor–patient relationship, is not an offer of treatment, and is not a recommendation to use or avoid any therapy. Neither compound is approved by the FDA for intravenous administration in any condition.

These statements have not been evaluated by the Food and Drug Administration. Individual results vary and no outcome is implied or promised. If you are undergoing treatment for cancer or any serious illness, discuss any additional therapy with your treating physician before starting it.

DMSO and DCA: What the Human Research Actually Shows