Cpi-613.
Research-backed compound with potential health benefits. It is not designed to boost energy or general health in normal people.
Reviewed March 2026
- Category
- Compound
What Cpi-613 is, and what it does.
- Does it work
- No. It is absolutely not for general use. Buying this from a grey market source is a terrible idea.
- How much to take
- Do not take this. Dosing is determined by oncologists in a clinical trial, often based on body surface area and administered under constant medical monitoring.
- Time to feel it
- It isn't a supplement with an onset. In hospital studies it's infused on a set schedule and what it does is tracked by scans and blood work rather than by sensation.
- The first dose
- In a clinical setting, patients can experience side effects like nausea or fatigue quite quickly. This is a potent drug, not a vitamin.
- With regular use
- Completely unknown for healthy individuals. The risks outside of a medical context have not been studied.
- How well tolerated
- Not established as well tolerated in public use. It's an Investigational New Drug (IND). Assume it carries significant risks until proven otherwise by regulatory bodies like the FDA.
- How it feels
- Like you're taking a serious experimental drug, because you are. Expect potential side effects, not health benefits. This is not a 'feel good' compound.
- The overlooked benefit
- It shares lipoic acid's eight-carbon backbone but not its cofactor job. Swapping the dithiolane ring for two benzylthio groups turns a helper into a blocker of the same enzymes.
500 to 1,000mg a day is where Cpi-613 works.
Source: Cancer Chemother Pharmacol. 2014;73(4):765-774. CPI-613 clinical trials.
The proof, claim by claim.
These words describe the research, not the molecule's worth. Research strength is how much work stands behind one claim, and it is never a product score.
Cpi-613 is documented in the library; the clinical read is in the queue. Nothing about the strength of the research prints until the read is done.
- inhibition of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenaseIn vitro study
- structural analogue relationship to endogenous lipoic acidNarrative review
- investigational intravenous administration under hospital supervisionRandomised trial
Questions people ask about Cpi-613.
- Is this just a stronger version of Alpha-Lipoic Acid (ALA)?
- No. It's an analog designed for a different, more aggressive purpose. Think of it as a specific weapon for a specific disease, not a general health tool.
- Can I buy Cpi-613 online?
- You might find it, but you absolutely should not buy it. It's illegal to sell as a supplement and incredibly dangerous. You have no idea what you're actually getting.
- What are the common side effects?
- Reported in clinical trials are fatigue, nausea, vomiting, and peripheral neuropathy (nerve tingling, numbness, or pain). The full side effect profile is still under investigation.
- Is this legal to take?
- It is an unapproved drug. Selling it as a supplement is illegal. Taking it outside of a doctor-supervised clinical trial is a significant health and legal risk.
Why these belong in the same formula. Each row says what the basis is, from settled biochemistry through to a trial that measured the pair.
CPI-613 is a lipoate analogue and engages the lipoylated E2 subunits of the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, the same positions lipoic acid occupies. Supplemental lipoate therefore competes at the site the analogue is designed to sit in.
The R enantiomer is the form the body attaches to the lipoyl domains of these enzyme complexes, so it is the direct natural counterpart to the analogue. The two act at one location rather than on separate pathways.
Thiamine pyrophosphate is the cofactor of the E1 subunit of both pyruvate dehydrogenase and the alpha-ketoglutarate complex, the two complexes the lipoate analogue engages. Thiamine status therefore sets baseline activity of the same machinery.
Blocking entry into and turnover of the TCA cycle reduces the NADH supply that feeds complex I, upstream of the point where coenzyme Q10 carries electrons. The two act on the same respiratory chain in sequence rather than at the same step. Read the relationship as mechanistic, not as a combination anyone should assemble.
The E3 subunit shared by pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase is FAD-dependent and derives that cofactor from riboflavin. A lipoate analogue acting at the lipoamide site interferes with the same catalytic cycle that riboflavin equips. Again the direction is opposing, not additive.
When pyruvate entry into the TCA cycle is constrained, cells lean more on fatty acid oxidation, which depends on carnitine-mediated transport of long-chain acyl groups into the mitochondrion. The relationship is one of metabolic compensation between two arms of the same organelle. It is inferred from established pathway biochemistry rather than measured together.
Both dehydrogenase complexes targeted by this compound reduce NAD+ to NADH, so inhibiting them changes the mitochondrial NAD+ to NADH ratio directly. Anything altering NAD availability sits on the same ledger. This is stoichiometric biochemistry, not a supplement pairing.
Lipoate and its analogues participate in thiol redox chemistry, and cellular glutathione status buffers the resulting shifts. Where mitochondrial redox is disturbed, glutathione is the main compensating thiol pool. The interaction is redox-level and does not imply a useful combination.
Nothing specific on file for Cpi-613. Match the label to the daily amount above, and tell your doctor what you take.
Not medical advice. Show the label to your pharmacist.What Cpi-613 actually does.
CPI-613 (devimistat) is a synthetic lipoic acid analogue, a 6,8-bis(benzylthio)octanoic acid, built on the same eight-carbon backbone as endogenous lipoate but with the dithiolane ring replaced by two benzylthio groups.
It acts at the lipoamide-dependent step of two mitochondrial dehydrogenase complexes, pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, which is why it is described as a mitochondrial metabolism inhibitor rather than a nutrient.
Because pyruvate dehydrogenase controls entry of pyruvate-derived acetyl-CoA into the TCA cycle and alpha-ketoglutarate dehydrogenase controls a rate-limiting step within it, blocking both constrains oxidative carbon flux at two points at once.
Endogenous lipoic acid is the covalently bound cofactor of these same complexes; the analogue relationship is structural, and a lipoate analogue does not carry lipoate's cofactor function.
Where Cpi-613 comes from.
It is made in a pharmaceutical plant from scratch, not extracted from anything. The starting chemicals are built up into the molecule, purified, and made into a sterile solution for hospital use in trials.
Chemically synthesised. The molecule is identical to the one a plant or an animal makes, and building it deliberately means a known purity, a fixed dose and no crop contaminants. For several nutrients this is the only route that reaches a usable amount.
Chemical synthesis starts from simple eight-carbon acid intermediates rather than from any biological lipoate source
Thiol groups at the 6 and 8 positions are benzylated to give 6,8-bis(benzylthio)octanoic acid, the structural change that separates it from natural lipoic acid
Recrystallisation and chromatographic purification to pharmaceutical impurity limits, with characterisation of related substances
Formulated for intravenous administration under pharmaceutical manufacturing controls for clinical study use
The essence, in one line each.
- In cultured cells, mitochondrial inhibition increased sensitivity to an oncolytic adenovirus; CPI-613 appears as one of the mitochondrial inhibitors named in the work.In vitro study. Shoji R et al., 2026 (Molecular Therapy: Oncology). PMID 42005830 ↗
- A methods protocol for assessing fasting metabolism and circadian clock coupling in mice, in which CPI-613 is named as a pyruvate dehydrogenase inhibitor tool compound.Animal study. Sun J et al., 2025 (STAR Protocols). PMID 39998953 ↗
- Work in daphnids linked pyruvate dehydrogenase activity to lifespan determination, using pharmacological inhibition of the complex as a probe.Animal study. Chen W et al., 2025 (Nature Communications). PMID 40188124 ↗
These are the studies our verdict leans on, chosen from the 3 we read for Cpi-613. The full linked list is below.
The studies, linked.
12 sources behind our Cpi-613 verdict: peer-reviewed studies and registered clinical trials. Every one links straight to PubMed, the journal, or ClinicalTrials.gov. Read them yourself.
- Clinical trialPhase 3 Multicenter Randomized Trial to Evaluate Efficacy and Safety of CPI-613 in Combination With HD Cyt. and Mito. vs HD Cyt. and Mito. Therapy and Control Sub-groups in Older Patients With R/R AMLClinicalTrials.gov ↗PHASE3 · 200 participants · Terminated
- Clinical trialA Multi-Center Randomized Phase IB/II Study of Gemcitabine and Cisplatin With or Without CPI-613 as First Line Therapy for Patients With Advanced Unresectable Biliary Tract Cancer (BilT-04)ClinicalTrials.gov ↗PHASE1 · 75 participants · Terminated
- Clinical trialA Phase II/I Open-Label Clinical Trial of CPI-613 in Combination With Modified FOLFIRINOX in Patients With Locally Advanced Pancreatic Cancer and Good Performance StatusClinicalTrials.gov ↗PHASE1 · 49 participants · Completed
- Clinical trialAn Open Label Study to Evaluate the Feasibility of CPI-613 Given With High Dose Cytarabine and Mitoxantrone in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML)ClinicalTrials.gov ↗PHASE1 · 48 participants · Completed
- Clinical trialAn Open Label, Dose-Escalation Study to Evaluate Safety, Tolerability, Maximum Tolerated Dose (MTD), Efficacy, and Pharmacokinetics (PKs) of CPI-613 Given Twice Weekly for Three Consecutive Weeks in Cancer PatientsClinicalTrials.gov ↗PHASE1 · 39 participants · Completed
- Clinical trialA Phase I Open-Label Dose-Escalation Clinical Trial of CPI-613 in Combination With Modified FOLFIRINOX in Patients With Metastatic Pancreatic Cancer and Good Performance StatusClinicalTrials.gov ↗PHASE1 · 21 participants · Completed
- Clinical trialA Phase I Clinical Trial of Fluorouracil (5-FU) + CPI-613 Combination in Previously Treated Metastatic Colorectal Cancer PatientsClinicalTrials.gov ↗PHASE1 · 19 participants · Completed
- Clinical trialA Pilot Open-Label Clinical Trial of CPI-613 in Patients With Advanced Bile Duct CancersClinicalTrials.gov ↗PHASE1 · 17 participants · Completed
- Clinical trialA Phase I/II Open-Label Trial of CPI-613® (Devimistat) Plus Hydroxychloroquine to Evaluate Maximally Tolerated Dose (MTD), Safety and Efficacy in Patients With Relapsed or Refractory Clear Cell Sarcoma of Soft TissueClinicalTrials.gov ↗PHASE1 · 16 participants · Completed
- Clinical trialPhase I Dose-Escalation Study of CPI-613, in Combination With Bendamustine, in Patients With Relapsed or Refractory T-Cell Non-Hodgkin Lymphoma or Classic Hodgkin LymphomaClinicalTrials.gov ↗PHASE1 · 16 participants · Completed
- Clinical trialA Phase I Dose-Escalation Study of CPI-613 (Devimistat) in Combination With Chemoradiation in Patients With Pancreatic AdenocarcinomaClinicalTrials.gov ↗PHASE1 · 8 participants · Terminated
- Clinical trialA Phase I/II Open-Label Dose-Escalation Clinical Trial of CPI-613 in Combination With Gemcitabine in Cancer PatientsClinicalTrials.gov ↗PHASE1 · 6 participants · Terminated
Evidence surfaced via Semantic Scholar (Allen Institute for AI) and ClinicalTrials.gov. Ranked by study type and citation weight, not cherry-picked.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.