The Naviaux Lab discovered that the unique properties of suramin made it the first in a new class of drugs that could be used to test the cell danger response (CDR) hypothesis for the origin and treatment of autism spectrum disorder (ASD).  Suramin successfully improved all the core symptoms of ASD and the metabolic and GI abnormalities in both animal models and a small human clinical trial. (PDF)


Suramin is not approved for any use in humans in the United States except to handle the few cases of African sleeping sickness (trypanosomiasis) that have recently traveled from Africa.  It is illegal to import suramin for human use without FDA approval.  It is illegal to use suramin in humans for any purpose in the US except in FDA-approved clinical trials.  Quoting from our 2017 publication, “Like many intravenous drugs, when administered improperly by untrained personnel, at the wrong dose and schedule, without careful measurement of drug levels and monitoring for toxicity, suramin can cause harm. Careful clinical trials will be needed over several years at several sites to learn how to use low-dose suramin safely in autism, and to identify drug–drug interactions and rare side effects that cannot currently be predicted. We strongly caution against the unauthorized use of suramin.”1 Homeopathic use of suramin is also illegal and untested. In addition, pharmaceutical grade suramin is hard to make.  Pure suramin is colorless when dissolved in water or saline as a 10% solution (100 mg/mL). Some batches of suramin contain impurities that are brown in color.  Brown-colored suramin should not be used.


Suramin was first synthesized by Bayer chemists in Germany in 1916.  Suramin is manmade and is not a natural product found anywhere in Nature. It is not found in pine needles and cannot be found in any herbal teas. The synthesis of suramin was an extension of Paul Ehrlich’s pioneering work that showed that certain chemical dyes were concentrated in microbial parasites like the trypanosomes that cause African sleeping sickness.

A drug Renaissance on the horizon

Dr. Naviaux frequently says, “Our work is not about suramin, or any other single drug.  Our research is aimed at discovering a completely new way to think about the cause and treatment of autism and dozens of other complex chronic disorders.” Suramin is just the first in a new class of drugs that will be synthesized to help regulate purinergic signaling.  Unfortunately, the importance of ATP and related metabolites in regulating the symptoms of disease and the stages of the healing cycle has only recently been recognized. Each of the 19 different purinergic receptors have different functions, and new roles for specific P2Y, P2X and P1 receptors are still being discovered.

New antipurinergic drugs (antagonists) and propurinergic drugs (agonists) are now being synthesized and tested but few have yet completed Phase 3 clinical trials and been approved.  The exceptions to this are the P2Y12 inhibitors like Plavix, which inhibit ADP-stimulated platelet aggregation.  Several P2Y12 inhibitors are approved to treat heart disease, but other purinergic receptors are likely to be more important in ASD. We were lucky that suramin is a non-selective inhibitor of most of the known types of purinergic receptors.  Now new drugs need to be made and studied individually that are selective for just one or two of the 19 purinergic receptors.

Graded amounts of extracellular ATP (eATP) are released from cells in proportion to stress.  The more stress, the more eATP is released. Stresses of all kinds are translated by the cell into graded eATP release.  Everything from high blood pressure, to psychological trauma, chemotherapy, surgery, toxin or pesticide exposure, stroke or heart attacks cause eATP to be released. One important way that stress-triggered eATP is released occurs through pannexin 1 containing channels in the cell membrane. New drugs to inhibit eATP release by regulating pannexin channels are being developed.  These pannexin channel blockers will likely be synergistic with anti-purinergic drugs in helping to reset, reboot, and support the completion of the healing cycle when it becomes stuck in any of the stages of the CDR.

Synergistic therapies

The goal will be to find synergistic therapies that can bring patients with chronic conditions through the stages of healing discussed above.  By facilitating the exit from the arrested mitochondrial progression needed to complete the healing cycle, recovery from chronic illnesses currently considered incurable may one day be possible. We envision a shelf-full of related drugs, a toolkit of devices, and a suite of new autonomic balancing, cognitive and behavioral therapies that can be matched to each patient and each disease.  It is our hope that each success will lay the groundwork for more successes, and soon there will be a drug, device, and therapeutic Renaissance that will create dozens of new tools that doctors can use to regulate the cell danger response and help patients heal.

Systematic clinical trials

  1. Autism spectrum disorder (ASD)
  2. Chronic Fatigue Syndrome (ME/CFS)
  3. Post-treatment Lyme disease syndrome (PTLDS)
  4. Post-coccidiomycosis (Valley fever) chronic fatigue syndrome
  5. Fragile X syndrome
  6. Treatment-Resistant Major Depressive Disorder with suicidal ideation
  7. NARP, Leigh, and other Primary Mitochondrial Diseases
  8. Post-traumatic stress syndrome (PTSD)
  9. Post-chemotherapy cognitive impairment, fragility, and accelerated aging symptoms
  10. Schizophrenia
  11. Chronic pain syndromes in children and adults
  12. Phantom limb pain
  13. Drug addiction recovery therapy, e.g., opioid addiction with hyperkatifeia
  14. Amyotrophic lateral sclerosis (ALS)
  15. Gulf War Illness (GWI)
  16. Treatment-resistant, post-COVID long-haulers with multisystem chronic fatigue syndrome
  17. Severe Obsessive-Compulsive Disorder (OCD)
  18. Lesch-Nyhan Syndrome (HPRT deficiency)
  19. Pediatric acute-onset neuropsychiatric syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS)
  20. Landau-Kleffner epilepsy
  21. Tourette’s syndrome
  22. As an additive in organ transplant media to improve organ survival, and decrease inflammation and rejection
  23. Generalized anxiety disorder (GAD)
  24. Subacute-chronic traumatic brain injury (TBI)
  25. Small fiber polyneuropathy (SFPN)
  26. Fibromyalgia
  27. Postural orthostatic tachycardia syndrome (POTS)/Dysautonomia
  28. Subacute spinal cord injury
  29. Early Parkinson disease
  30. Early Alzheimer dementia

Suramin updates

Suramin was shown to be safe and effective in three preclinical models of ASD9-11 and a small human clinical trial1 in peer-reviewed papers published between 2013-2017. Further development of suramin was passed from Dr. Naviaux’s university research lab to the private sector.  Dr. Naviaux no longer has any control over the next clinical studies or the priorities of different diseases for testing, although he is recommending ASD, ME/CFS, post-acute SARS-CoV-2 multi-system chronic fatigue syndrome, also called long-COVID, and post-treatment Lyme disease (PTLDS) as a few of the top candidates.


  1. Naviaux, R.K., et al. Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical trial. Ann Clin Transl Neurol 4, 491-505 (2017).
  2. Naviaux, R.K. & Nguyen, K.V. POLG Mutations Associated with Alpers’ Syndrome and Mitochondrial DNA Depletion. Annals of neurology 55, 706-712 (2004).
  3. Naviaux, R.K., et al. Mitochondrial DNA polymerase gamma deficiency and mtDNA depletion in a child with Alpers’ syndrome. Annals of neurology 45, 54-58 (1999).
  4. Graf, W.D., et al. Autism associated with the mitochondrial DNA G8363A transfer RNA(Lys) mutation. Journal of child neurology 15, 357-361 (2000).
  5. Gourley, P.L., et al. Reactive biomolecular divergence in genetically altered yeast cells and isolated mitochondria as measured by biocavity laser spectroscopy: rapid diagnostic method for studying cellular responses to stress and disease. J Biomed Opt 12, 054003 (2007).
  6. Gourley, P.L. & Naviaux, R.K. Optical phenotyping of human mitochondria in a biocavity laser. IEEE J. Selected Topics Quantum Electronics 11, 818-826 (2005).
  7. Gourley, P.L., et al. Ultrafast nanolaser flow device for detecting cancer in single cells. Biomed Microdevices 7, 331-339 (2005).
  8. Naviaux, R.K., et al. Retained features of embryonic metabolism in the adult MRL mouse. Molecular genetics and metabolism 96, 133-144 (2009).
  9. Naviaux, J.C., et al. Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model. Molecular autism 6, 1 (2015).
  10. Naviaux, J.C., et al. Reversal of autism-like behaviors and metabolism in adult mice with single-dose antipurinergic therapy. Translational psychiatry 4, e400 (2014).
  11. Naviaux, R.K., et al. Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model. PloS one 8, e57380 (2013).