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Diacca is diAcCA, the di-acetylated form of carnosic acid, the phenolic diterpene that gives rosemary and sage most of their pharmacology. Purified carnosic acid oxidises readily and is too unstable to develop as a drug, which is the problem the acetyl groups solve: they make a stable solid that converts back to carnosic acid in the stomach before anything is absorbed [1]. What then circulates is carnosic acid, a pro-electrophile that becomes an electrophilic quinone under oxidation and alkylates cysteine thiols on Keap1, releasing Nrf2 to turn on the phase 2 antioxidant genes [2]. The compound was built at Scripps specifically as an Alzheimer's candidate, and in 5xFAD transgenic mice given it for three months it rescued synapses, improved water maze learning and reduced amyloid plaque, phospho-tau aggregates and glial inflammation [1]. That paper is the whole published record for diAcCA itself. Everything else known about the molecule is known about carnosic acid, which is a fair inference here because carnosic acid is what the prodrug becomes, but it is still an inference.
- No substantiated benefits; the compound's identity and effects are undocumented
- Listed only as generic research material, so any purported benefit is unverified
- Not established in humans; no adverse event data exist for diAcCA
- Gastrointestinal effects are a documented consequence of the released carnosic acid, which inhibits gastric lipase and cut fat absorption in rats
- High doses of the parent herb significantly impaired speed of memory in older adults in the one dose-ranging trial, so a larger amount is not a safer bet
Overview
No credible scientific source was found that defines what Diacca is, how it works, or what effects it produces. It appears in research-chemical catalogues as a powder and capsule product marketed for laboratory use, but without a certificate-of-analysis structure, an established chemical name, a CAS number, or any published study, its identity remains genuinely uncertain.
In the interest of honesty, this entry does not attribute a mechanism, benefits or dosing to Diacca that cannot be substantiated. Anyone encountering it should treat it as an unknown substance: identity and purity cannot be assumed, there is no human or preclinical evidence base, and no safety profile exists. Independent laboratory analysis would be required before any meaningful characterization could be offered.
- No public scientific source clearly defines what Diacca actually is, which is unusual even among obscure research chemicals.
- Its name is sometimes guessed to imply a diacetyl or diacetate derivative, but this remains unconfirmed speculation.
Mechanism
Carnosic acid is not electrophilic as it sits. It carries a catechol ring that becomes an electrophilic quinone only once oxidised, and that is the entire design idea: the molecule activates where already exists and stays inert elsewhere, which is what separates it from a permanently electrophilic drug like dimethyl fumarate [3] [4]. Once oxidised it alkylates specific cysteine thiols on Keap1, the sensor protein that normally holds Nrf2 in the cytoplasm for degradation.
Nrf2 is freed, enters the nucleus and drives the antioxidant response element, switching on the phase 2 genes: NQO1, both cysteine ligase subunits that build glutathione, and the cystine transporter xCT [2] [6]. The practical output is a rise in reduced glutathione and in enzymatic antioxidant capacity rather than direct radical scavenging, which is why the effect takes time and why it does not look like a dose of vitamin C [7].
Downstream of NRF2, the same activation restrains the NLRP3 inflammasome, the proposed route to the anti-inflammatory effect seen on and astrocytes [5] [6]. Carnosic acid crosses the blood brain barrier and reaches brain parenchyma, and raises brain glutathione in vivo [2] [5]. The acetyl groups on diAcCA contribute none of this; they exist only to stop the molecule oxidising on the shelf, and they are hydrolysed off in the stomach before absorption [1].
Carnosic acid also carries activity unrelated to Nrf2: it is a micromolar at human PPAR gamma [9], and it inhibits gastric lipase, which is the proposed reason a rosemary extract standardised to carnosic acid slows weight gain and lowers serum triglycerides, cholesterol and in rats [10].
receptor fingerprint
Keap1Covalent S-alkylation of specific sensor cysteine thiols by the oxidised quinone form of carnosic acid
Nrf2 and the antioxidant response elementPathway activation; induction of the phase 2 genes NQO1, GCLC, GCLM and xCT
NLRP3 inflammasomeRestrained downstream of NRF2 activation
Gastric lipaseInhibition in the stomach, where intact carnosic acid concentrates
PPAR gammaDirect agonist in a human receptor reporter assay
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
There is no human safety data for diAcCA. The one published study reports that in rodent toxicity work diAcCA was as safe as or safer than carnosic acid itself, and notes that carnosic acid is listed by the FDA as generally regarded as safe [1]; specific rosemary extract compositions are accepted by both the FDA and EFSA as antioxidant food additives [11].
That is a food-additive record at culinary exposure, not a drug safety record at a therapeutic dose, and treating the first as the second is the main error available here. Three published findings are worth holding onto. Carnosic acid inhibits three human enzymes in vitro, glutathione S-transferase, glutathione reductase and paraoxonase 1, at high micromolar concentrations [12]; two of those sit inside the same glutathione system the compound is meant to support, which is a tension nobody has resolved in vivo.
Carnosic acid inhibits gastric lipase in rats strongly enough to reduce fat absorption and body weight gain [10], so a gastrointestinal effect is a documented consequence rather than a theoretical one. And the only dose-ranging human trial of the parent herb found a biphasic result: the lowest dose improved speed of memory while the highest dose significantly impaired it, with scattered deleterious effects on other cognitive measures [13], which is a direct warning that more is not better with this chemistry. Nothing available amounts to a toxicology package for diAcCA. Not medical advice.
History
Carnosic acid has been a serious neuroprotection candidate since 2007, when Satoh, Lipton and colleagues showed it activates the Keap1/Nrf2 pathway by alkylating specific Keap1 cysteines, raises reduced glutathione in vivo, crosses into brain and protects rodent brain against middle cerebral artery ischaemia and reperfusion [2].
The obstacle was never the pharmacology; it was the molecule, because purified carnosic acid oxidises readily and is highly unstable [1]. Through the 2010s the same group built a general argument for pro-electrophilic drugs, compounds inert until oxidative stress converts them, as a way to get the benefit of an Nrf2 activator without the non-specific thiol alkylation and glutathione depletion that give dimethyl fumarate its systemic side effects [3] [4].
The case was then extended to Parkinson's disease and to the NLRP3-driven inflammation implicated in long COVID [5]. diAcCA is the answer to the stability problem: acetylate both phenols and let the stomach cleave them. It was published in 2025 out of the Neurodegeneration New Medicines Center at Scripps, with Phil Baran's chemistry group involved, and the paper closes by arguing that the compound is suitable for human clinical trials in Alzheimer's disease [1]. No such trial has started.
Reputation
Almost none, and what exists is a year old. The 2025 mouse paper drew mainstream science press coverage as a rosemary-derived Alzheimer's candidate, and research-chemical vendors listed the compound shortly afterwards as a powder and in capsules for laboratory use. There is no community of long-term users, no body of self-reported experience worth weighing, and no independent replication of the animal result. Carnosic acid itself has a longer and better reputation, mostly as a food antioxidant and as the interesting fraction of rosemary extract, and a reader tempted by diAcCA is really being tempted by carnosic acid with a better shelf life. Anyone selling it is selling ahead of the evidence, which is the ordinary condition of a compound that got one good paper and a headline.
Resources
This entry is here for reference.
Research
- 2006first citedCarnosic acid and carnosol, phenolic diterpene compounds of the labiate herbs rosemary and sage…
- 2012most active year3 papers
- 2025most recentdiAcCA, a Pro-Drug for Carnosic Acid That Activates the Nrf2 Transcriptional Pathway, Shows Eff…
- 1.diAcCA, a Pro-Drug for Carnosic Acid That Activates the Nrf2 Transcriptional Pathway, Shows Efficacy in the 5xFAD Transgenic Mouse Model of Alzheimer's Disease.
- 2.Carnosic acid, a catechol-type electrophilic compound, protects neurons both in vitro and in vivo through activation of the Keap1/Nrf2 pathway via S-alkylation of targeted cysteines on Keap1.
- 3.Nrf2/ARE-mediated antioxidant actions of pro-electrophilic drugs.
- 4.Recent advances in understanding NRF2 as a druggable target: development of pro-electrophilic and non-covalent NRF2 activators to overcome systemic side effects of electrophilic drugs like dimethyl fumarate.
- 5.Potential Therapeutic Use of the Rosemary Diterpene Carnosic Acid for Alzheimer's Disease, Parkinson's Disease, and Long-COVID through NRF2 Activation to Counteract the NLRP3 Inflammasome.
- 6.Carnosic acid, a pro-electrophilic compound, inhibits LPS-induced activation of microglia.
- 7.Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action.
- 8.Carnosic acid protects against 6-hydroxydopamine-induced neurotoxicity in in vivo and in vitro model of Parkinson's disease: involvement of antioxidative enzymes induction.
- 9.Carnosic acid and carnosol, phenolic diterpene compounds of the labiate herbs rosemary and sage, are activators of the human peroxisome proliferator-activated receptor gamma.
- 10.Inhibition of gastric lipase as a mechanism for body weight and plasma lipids reduction in Zucker rats fed a rosemary extract rich in carnosic acid.
- 11.Rosemary (Rosmarinus officinalis L.) Extract as a Potential Complementary Agent in Anticancer Therapy.
- 12.Inhibitory Effects of Usnic and Carnosic Acid on Some Metabolic Enzymes: An In vitro Study.
14 listed here; entry last updated July 2026
Reviews
My notesprivate to this device
FAQ
What is Diacca?
Its chemical identity is not documented in any reliable scientific source. It is sold as a research-chemical powder, and speculation that the name implies a diacetyl or diacetate derivative is unconfirmed.
Is it safe to take Diacca?
There is no way to know. With no established identity, purity standard or safety data, it should be treated as an unknown substance and is sold for laboratory research only.
What actually is Diacca?
diAcCA, the di-acetylated form of carnosic acid, the phenolic diterpene found in rosemary and sage. The two acetyl groups are a shelf-stability device rather than a pharmacological one; they are cleaved in the stomach, and what reaches the bloodstream is carnosic acid [1]. The older description of this compound as an unidentified research-chemical powder was wrong.
Is it any different from just taking carnosic acid or rosemary extract?
The delivered molecule is the same, so the pharmacology should be the same. The difference is stability: purified carnosic acid oxidises readily and diAcCA does not, and the developers report improved stability and bioavailability with comparable pharmacokinetics and comparable efficacy [1]. Whether that gap matters at the exposures a person would actually use has never been tested in people.
Has anyone taken it?
Not in any published or registered study. No clinical trial of diAcCA appears on ClinicalTrials.gov, and the entire published record for the compound is one 2025 mouse study in a transgenic Alzheimer's model [1]. The nearest human evidence is on whole rosemary, which delivers carnosic acid alongside carnosol, rosmarinic acid and ursolic acid and cannot be attributed to any single one of them [14] [13].
Will it help my memory?
Unknown. It improved learning and memory in 5xFAD mice, an aggressive model carrying five familial Alzheimer's mutations that loses synapses, and the improvement came with measured synaptic rescue [1]. That is a rescue of pathology, and rescuing a damaged system does not imply improving a healthy one. Working against the optimistic reading, the only dose-ranging human trial of the parent herb found that the highest dose significantly impaired speed of memory [13].
Does it interact with anything I might already be taking?
No interaction work exists for diAcCA specifically. Two published findings are relevant. Carnosic acid inhibits glutathione S-transferase, glutathione reductase and paraoxonase 1 in vitro at high micromolar concentrations [12], which touches drug metabolism and the body's own antioxidant enzymes. And it inhibits gastric lipase enough to cut fat absorption in rats [10], which could plausibly affect fat-soluble vitamins or supplements taken at the same time. Neither has been checked in a person. Not medical advice.
Why is it sold as a research chemical if it is basically rosemary?
Because diAcCA is a synthetic derivative, not a food constituent. Carnosic acid occurs in rosemary and specific rosemary extract compositions are accepted as food additives by the FDA and EFSA [11]; the di-acetylated prodrug is a new chemical entity that has never been through a regulatory review, has no approved use and has never been given to a person under a protocol [1]. Vendors label it for laboratory research only.
Limitations of the evidence
- The entire evidence base for diAcCA itself is a single 2025 mouse study; every other citation in this entry is about carnosic acid, the molecule the prodrug becomes, or about whole rosemary
- No registered clinical trial exists, so there is no human dose, no human pharmacokinetics and no human safety data
- The animal model is 5xFAD, an aggressive transgenic mouse carrying five familial Alzheimer's mutations; a result in it is a claim about that model, not about sporadic Alzheimer's disease in people
- No independent group has replicated the diAcCA result
- The human evidence nearest to it uses whole rosemary leaf or extract, which delivers several active constituents at once and cannot isolate carnosic acid
- Carnosic acid inhibits glutathione S-transferase and glutathione reductase in vitro, which sits awkwardly beside the claim that its main benefit is supporting the glutathione system; nobody has reconciled the two in a living animal
Adverse effects
- Not established in humans; no adverse event data exist for diAcCA
- Gastrointestinal effects are a documented consequence of the released carnosic acid, which inhibits gastric lipase and cut fat absorption in rats
- High doses of the parent herb significantly impaired speed of memory in older adults in the one dose-ranging trial, so a larger amount is not a safer bet
Notes and cautions
- Unknown; no safety data exist for an unidentified compound
- Sold by Umbrella Labs as a 5 gram powder and as 100 mg capsules, labelled for laboratory research only
- PubChem CID 13966132; CAS 3650-24-6; molecular formula C24H32O6
- The acetyl groups are cleaved in the stomach, so the molecule that reaches the blood is carnosic acid rather than diAcCA
- Developed at the Neurodegeneration New Medicines Center, The Scripps Research Institute; the 2025 paper is open access in Antioxidants