DAPTA
An eight-amino-acid fragment of HIV's own envelope protein, tested in the 1990s against AIDS dementia, nerve pain and psoriasis
DAPTA is a short synthetic peptide copied from a stretch of gp120, the outer protein HIV uses to latch onto cells. Swapping its first amino acid for the mirror-image D-alanine and capping its tail as an amide made it last longer in the body than its parent, peptide T. Researchers first thought it worked at CD4; later lab work showed it sits on CCR5, the co-receptor most HIV strains need to get in. Given as a nasal spray, it failed the main goal of its two placebo-controlled trials, in HIV-related cognitive problems and in painful neuropathy, though some subgroups did better. Small studies also tried it in psoriasis. It was never approved anywhere.
Used in human trials: 2 mg, Three times a day, Intranasal spray (Study: HIV-associated cognitive impairment) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
Work out syringe units → · New to syringes? · All dosing data ↓ · Dose and vial tracker · Is this vial OK?
What is it?
In 1986 researchers at the US National Institute of Mental Health went looking for the part of HIV's envelope protein, gp120, that might grip a receptor in the brain. They picked out an eight-residue stretch rich in threonine, Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr, and called it peptide T after that letter. Peptide T itself is the parent molecule and has no page here, because the people in the trials were given a modified copy instead. That copy, DAPTA, carries D-alanine, the mirror form of the first amino acid, and an amide on the last one. Both changes make it harder for enzymes to chew up, and the developers later used the name Adaptavir for it.
For its first decade DAPTA was believed to act at CD4, the main HIV receptor on T cells, and several groups could not reproduce its antiviral effect. The explanation came after chemokine co-receptors were discovered. The laboratory strain everyone was testing used CXCR4, while DAPTA turned out to block CCR5, the co-receptor used by the strains that dominate early infection and the brain. Binding studies in 2005 found it kept gp120 off CCR5 at sub-nanomolar concentrations, and in 2007 a group in Rome found it stopped HIV from entering infected macrophages.
The early trials focused on the brain. HIV can damage thinking and movement, and DAPTA had protected neurons from gp120 in cell culture. An open phase 1 study gave it into a vein and then as a nasal spray to 14 people with AIDS or AIDS-related complex. The larger test was a three-site, placebo-controlled trial of 2 mg sprayed into the nose three times a day for six months in people with HIV and cognitive impairment. It showed no overall benefit. Patients with clearer impairment, or with CD4 counts above 200, appeared to do better, but these were subgroup findings. A trial in painful HIV neuropathy found no difference from placebo at all.
Later work went back to the blood. Re-testing stored samples from the cognition trial suggested DAPTA had lowered virus in the blood but not in the spinal fluid. A small open study in 11 long-infected patients reported fewer infected monocytes and more interferon-producing T cells. A phase 2 trial of a monomeric form in people already on antiretroviral therapy was registered in 2009; it has posted no results.
A separate line of work tried it for psoriasis. Infused directly into plaques, it cleared them more than saline did in the same patients, and in a 28-day intravenous study most patients improved. More recent animal studies have used DAPTA as a CCR5 blocker in models of Alzheimer-type brain inflammation, multiple sclerosis and autism. None of this has led to an approved product. Every human dose listed below comes from a study.
Mechanism of Action
DAPTA mimics a piece of HIV's envelope and occupies the CCR5 co-receptor, so the virus and some inflammatory signals that use CCR5 are kept out; its two chemical changes slow its breakdown.
Sits on CCR5
It blocks gp120, already bound to CD4, from docking onto CCR5 at sub-nanomolar concentrations, and a labelled copy binds only cells that carry CCR5 (PMID 16002156).
Keeps CCR5-using HIV out
In infected macrophages it stopped viral entry and cut replication by over 90%, with no effect on the CXCR4-using laboratory strain that confused early researchers (PMIDs 18046961, 15043212).
Shields neurons and calms glia
It prompts astrocytes to release protective chemokines in culture (PMID 10446313) and reduced activated microglia and astrocytes in an inflamed rat brain (PMID 15979806).
Slower to break down
D-alanine and the C-terminal amide resist enzymes that trim peptides from the ends; in the gut it is still cut mainly by enkephalinase (PMID 7654767), and in blood it clears in two phases (PMID 1763193).
Published Research
The studies behind DAPTA, read from their PubMed abstracts: the human trials in HIV-related cognitive impairment, neuropathy and psoriasis, its pharmacokinetics, a 2003 review, and the animal and cell studies of its CCR5 blocking. Six human records title the drug 'peptide T'; each is carded because its abstract states that the D-Ala amide was given.
Cognitive impairment in HIV: the main trial
At three sites, HIV-positive people with cognitive deficits took 2 mg intranasally three times daily or placebo for six months. The global neuropsychological score did not differ between groups. Exploratory analyses favoured the drug in people with CD4 counts above 200 cells/µL or more marked impairment, and decline was more common on placebo in that second group.
Viral load in the same trial
A retrospective look at participants who completed six months measured HIV RNA in spinal fluid (92 people) and in plasma or serum (57). Virus in the blood fell more in the DAPTA group, while spinal fluid levels did not differ. The authors called for confirmation.
Painful HIV neuropathy
In 81 evaluable patients with painful distal neuropathy, 6 mg a day intranasally for 12 weeks relieved pain no better than placebo, and nerve tests, cognition and CD4 counts did not change. No significant drug-related adverse effects were seen.
Viral reservoirs in long-term infection
Eleven patients infected for an average of 17 years took the nasal spray for up to 32 weeks. Plasma HIV RNA did not change, but less virus could be grown from their white cells over time, and most monocyte reservoirs became undetectable. Five had CD4 rises averaging 33%. There was no control group.
Extended phase 1 in AIDS and ARC
Fourteen patients received 0.1 to 3.2 mg/kg a day into a vein for 12 weeks; six then used 25 mg a day intranasally for 8 weeks. Toxicity was minimal. Patients with moderate impairment did better on cognitive and motor tests than untreated controls, and weight rose about 2 kg, while immune and viral measures did not change.
How long it stays in the blood
In the phase 1 patients, plasma levels fell in two phases, a first half-life of 30 to 60 minutes and a second of 4 to 6 hours, after both intravenous and nasal doses. Spinal fluid levels reached about 20% of plasma in two people, none appeared in urine, and the spray was tolerated for up to 21 months.
Psoriasis: infused into plaques
Fourteen patients each had one plaque infused with DAPTA at 10^-7 mol/L by a small pump for two weeks and a matched plaque with saline. Clinical scores fell from about 4.4 to 1.6 on the drug against 4.4 to 3.6 on saline, and biopsies also scored better.
Psoriasis: skin changes during IV treatment
Ten psoriasis patients received 2 mg a day intravenously for 28 days and most improved. Serial biopsies showed large shifts in somatostatin-containing dendritic cells in the skin, which the authors propose as part of how lesions healed. Uncontrolled.
Review by its discoverers
Traces DAPTA from its 1986 discovery as a gp120 fragment through the failed attempts to reproduce its antiviral effect, explained later by its selectivity for CCR5 over the laboratory strain's receptor. It summarises early trials showing little toxicity and presents cytokine and T-cell data from a small phase 2 study.
Brain inflammation (rats)
In rats given a chronic infusion of bacterial endotoxin into the brain, a model of Alzheimer-type inflammation, 0.01 mg/kg under the skin for 14 days sharply cut the number of activated microglia and astrocytes in the hippocampus and lowered NF-κB-positive cells.
Multiple sclerosis model (mice)
Mice with experimental autoimmune encephalomyelitis received 0.01 mg/kg daily by injection into the abdomen from day 14 to day 42. Inflammatory signals including NF-κB p65, Notch-1, Notch-3, TNF-α and iNOS fell in spleen B cells and in brain tissue.
Autism-like behaviour (mice)
In BTBR mice, a strain with autism-like traits, 0.01 mg/kg daily for 7 days reduced marble burying and repetitive behaviour, lowered IL-17A and IL-9 immune signals, and raised the anti-inflammatory IL-10 and Foxp3.
Crossing into the brain
A radio-iodinated copy injected into the bloodstream reached the brain intact, more than an albumin control did, despite very low fat solubility. Unlabelled peptide slowed its entry, pointing to a saturable transport system; no such system carried it back out.
Breakdown in the gut
In rabbit intestinal membranes the peptide was cut mainly by enkephalinase and partly by aminopeptidases; blocking the first enzyme stopped 85% of the breakdown. In perfused rat gut more of it survived at acidic pH, suggesting oral absorption might be possible if digestion were held back.
CCR5 identified as its receptor
DAPTA blocked CD4-dependent binding of two gp120 variants to CCR5 at IC50 values of 0.06 and 0.32 nM, stopped the gp120-CD4 complex from joining CCR5 at 1 nM, and a fluorescent copy bound cells carrying CCR5 but not cells lacking it.
Blocking HIV in macrophages
At 10^-9 M it cut replication of CCR5-using HIV in monocytes and macrophages by more than 90% by stopping entry, and it protected a neuroblastoma cell line from virus-induced cell death better than the small-molecule CCR5 blocker TAK-779.
Protecting neurons through chemokines
In rat brain cultures, DAPTA and VIP prevented neuron death caused by five gp120 variants. Treated astrocytes released the chemokines MIP-1α and RANTES, which on their own also shielded neurons from gp120.
Dosing Data
Every human dose of DAPTA was given inside a study: mostly as a nasal spray, sometimes into a vein or straight into a skin lesion. These are the amounts those studies used; there is no approved dose.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes DAPTA is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: intranasal spray, intravenous). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store DAPTA, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long DAPTA stays intact once mixed.
How it is taken
As it was given in human studies: Intranasal spray (Three times a day; Study: HIV-associated cognitive impairment); Intravenous, then intranasal (Daily; Study: phase 1 in AIDS and ARC); Intravenous (Daily; Study: psoriasis).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of 30-60 minutes (first phase) then 4-6 hours (second phase) after intravenous or intranasal dosing. After about five half-lives almost none is left.
How long the doses were given: Study: HIV-associated cognitive impairment: 6 months; Study: painful HIV neuropathy: 12 weeks; Study: phase 1 in AIDS and ARC: 12 weeks intravenous, then 8 weeks intranasal.
When effects appear: unknown; no source on this page gives a time to effect for DAPTA. Results reported in the studies are under Published Research.
Source: half-life: PMID 1763193; Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: No significant drug-related adverse effects in either group of the 12-week neuropathy trial (PMID 8909439); Minimal evidence of toxicity over 12 weeks of intravenous dosing in phase 1 (PMID 1775594); The nasal spray was tolerated for up to 21 months in the phase 1 patients (PMID 1763193); No drug-related toxicity reported over up to 32 weeks in 11 long-infected patients (PMID 14499289). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping DAPTA. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the studies above”).
Interactions
Unknown: a PubMed search for human interaction studies of DAPTA (reviewed 2026-11-03) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of DAPTA products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against DAPTA's expected mass, 856.9 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Not FDA Approved (Never approved: Drugs@FDA (openFDA) holds no application for DAPTA, Adaptavir or peptide T (searched November 3, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
From the studies above. None reported a serious drug-related problem, but all were small or short.
Contraindications & Cautions
There is no label. These cautions follow from how and where it was tested.
Legal Status
DAPTA is an investigational drug that never reached the market.
Frequently Asked Questions
?What is DAPTA?
A synthetic eight-amino-acid peptide copied from a piece of HIV's envelope protein gp120, carrying a D-alanine at the start and an amide at the end. It occupies the CCR5 co-receptor that most HIV strains use to get into cells.
?Is DAPTA the same as peptide T?
Not quite. Peptide T is the original fragment. DAPTA is its modified, longer-lasting form, and it is the version actually given in the human studies, which often still called it peptide T.
?Did it help HIV-related memory and thinking problems?
Not for the trial group as a whole. The six-month placebo-controlled trial missed its main outcome. Only subgroups, such as people with higher CD4 counts or more marked impairment, seemed to benefit.
?How was it given?
Mostly as a nasal spray in the HIV trials. Early phase 1 work used an intravenous drip, and the psoriasis studies infused it into the skin or gave it into a vein.
?Can I buy DAPTA?
No. It was never approved or marketed anywhere and was only ever supplied to people inside research studies.
References
- [clinical-trial] Heseltine PN, et al. "Randomized double-blind placebo-controlled trial of peptide T for HIV-associated cognitive impairment." Arch Neurol, 1998;55(1):41-51. PMID: 9443710.
- [clinical-trial] Goodkin K, et al. "Cerebrospinal and peripheral human immunodeficiency virus type 1 load in a multisite, randomized, double-blind, placebo-controlled trial of D-Ala1-peptide T-amide for HIV-1-associated cognitive-motor impairment." J Neurovirol, 2006;12(3):178-89. PMID: 16877299.
- [clinical-trial] Simpson DM, et al. "Peptide T in the treatment of painful distal neuropathy associated with AIDS: results of a placebo-controlled trial. The Peptide T Neuropathy Study Group." Neurology, 1996;47(5):1254-9. PMID: 8909439.
- [clinical-trial] Polianova MT, et al. "Antiviral and immunological benefits in HIV patients receiving intranasal peptide T (DAPTA)." Peptides, 2003;24(7):1093-8. PMID: 14499289.
- [clinical-trial] Bridge TP, et al. "Results of extended peptide T administration in AIDS and ARC patients." Psychopharmacol Bull, 1991;27(3):237-45. PMID: 1775594.
- [clinical-trial] Ruff MR, et al. "Pharmacokinetics of peptide T in patients with acquired immunodeficiency syndrome (AIDS)." Prog Neuropsychopharmacol Biol Psychiatry, 1991;15(6):791-801. PMID: 1763193.
- [clinical-trial] Farber EM, et al. "Peptide T improves psoriasis when infused into lesions in nanogram amounts." J Am Acad Dermatol, 1991;25(4):658-64. PMID: 1791224.
- [clinical-trial] Johansson O, et al. "Somatostatin immunoreactive cells in lesional psoriatic human skin during peptide T treatment." Acta Derm Venereol, 1994;74(2):106-9. PMID: 7911613.
- [review] Ruff MR, et al. "Update on D-ala-peptide T-amide (DAPTA): a viral entry inhibitor that blocks CCR5 chemokine receptors." Curr HIV Res, 2003;1(1):51-67. PMID: 15043212.
- [pubmed] Rosi S, et al. "Chemokine receptor 5 antagonist D-Ala-peptide T-amide reduces microglia and astrocyte activation within the hippocampus in a neuroinflammatory rat model of Alzheimer's disease." Neuroscience, 2005;134(2):671-6. PMID: 15979806.
- [pubmed] Alghibiwi H, et al. "DAPTA, a C-C Chemokine Receptor 5 (CCR5), Leads to the Downregulation of Notch/NF-κB Signaling and Proinflammatory Mediators in CD40(+) Cells in Experimental Autoimmune Encephalomyelitis Model in SJL/J Mice." Biomedicines, 2023;11(6). PMID: 37371605.
- [pubmed] Ahmad SF, et al. "DAPTA, a C-C chemokine receptor 5 (CCR5) antagonist attenuates immune aberrations by downregulating Th9/Th17 immune responses in BTBR T(+) Itpr3tf/J mice." Eur J Pharmacol, 2019;846:100-108. PMID: 30658114.
- [pubmed] Barrera CM, et al. "D-[Ala1]-peptide T-amide is transported from blood to brain by a saturable system." Brain Res Bull, 1987;19(6):629-33. PMID: 3440215.
- [pubmed] Su SF, et al. "Investigation into the intestinal metabolism of [D-Ala1] peptide T amide: implication for oral drug delivery." Biochim Biophys Acta, 1995;1245(1):62-8. PMID: 7654767.
- [pubmed] Polianova MT, et al. "Chemokine receptor-5 (CCR5) is a receptor for the HIV entry inhibitor peptide T (DAPTA)." Antiviral Res, 2005;67(2):83-92. PMID: 16002156.
- [pubmed] Pollicita M, et al. "Profound anti-HIV-1 activity of DAPTA in monocytes/macrophages and inhibition of CCR5-mediated apoptosis in neuronal cells." Antivir Chem Chemother, 2007;18(5):285-95. PMID: 18046961.
- [pubmed] Brenneman DE, et al. "VIP and D-ala-peptide T-amide release chemokines which prevent HIV-1 GP120-induced neuronal death." Brain Res, 1999;838(1-2):27-36. PMID: 10446313.
- [registry] ClinicalTrials.gov API v2, read November 3, 2026: NCT00951743 (phase 2, Adaptavir (monomeric DAPTA) 0.01 mg intranasally twice a day against placebo for 24 weeks in people with HIV whose plasma virus was suppressed by antiretroviral therapy; 40 planned; started July 2009, last status 'unknown', no results posted). https://clinicaltrials.gov/study/NCT00951743
- [other] PubChem CID 184644 ('Dapta'; synonyms Adaptavir, RAP101, (D-Ala1)-peptide T amide, D-Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr-NH2): molecular formula C35H56N10O15, molecular weight 856.9. Read November 3, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/184644
- [other] US FDA, Drugs@FDA (openFDA drugsfda endpoint), searched November 3, 2026: no application for DAPTA, Adaptavir or peptide T.
Sources & Citations
Every study on this page was read from its PubMed record on November 3, 2026. The trial registration comes from ClinicalTrials.gov, structure and formula from PubChem, and regulatory status from Drugs@FDA, read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.