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Dipyridamole

Platelet aggregation inhibitors excl. heparin · given by injection, oral · on the market since 1990

5
Leads
24.5M
People
8
Makers
63
How abandoned
01

What it's made of

Each functional group on the molecule does a specific, predictable job.

No standard functional groups matched.

02

Where it can get to

Predicted from molecular weight, lipophilicity, polar surface area and hydrogen-bond donor count. A drug can only act where it distributes, so this constrains which conditions are addressable before any biology is considered. derived

Partly
Systemic circulation
Absorbed from the gut and distributed in plasma.
No
Central nervous system
Crosses the blood–brain barrier.
Partly
Intestinal lumen only
Poorly absorbed. Acts locally in the gut with minimal systemic exposure.
No
Skin
Crosses the stratum corneum. Viable as a topical.
Partly
Urinary tract
Cleared unchanged in urine. Local concentration exceeds plasma.
03

What it binds — and whether we can reach it · 6 of 7 reachable

Binding affinity is only meaningful against the plasma concentration reached at the approved dose. A target requiring higher concentrations cannot be engaged in a patient, whatever the in vitro potency. Most repurposing hypotheses fail at this step, and it is rarely checked before a trial is proposed. measured

Values are pAct — the negative logarithm of the molar concentration at which the drug half-occupies the target. Each whole step is a tenfold difference in potency: 9.0 = 1 nanomolar, 6.0 = 1 micromolar, 5.0 = 10 micromolar. Oral drugs typically reach 0.1–10 micromolar in plasma, so roughly 6.0 is the threshold below which a target cannot be reached at a tolerated dose. Figures come from DrugCentral’s curated binding data.
SLC29A1
Transporter · inhibitor
8.5
Engaged easily
PDE6D
Enzyme · inhibitor
6.9
Just reachable
PDE5A
Enzyme · inhibitor
6.28
Just reachable
PDE7A
Enzyme · inhibitor
6.22
Just reachable
PDE10A
Enzyme · inhibitor
6
Just reachable
PDE7B
Enzyme · inhibitor
6
Just reachable
PDE4A
Enzyme · inhibitor
5.8
Out of reach

This molecule concentrates in urine. Local concentration therefore exceeds plasma, so targets that look unreachable on a plasma reading may still be engaged. assumed

04

New uses, and who is already trying them

One card per candidate indication: the reasoning link by link, the evidence tier that governs how strongly it can be stated, and any registered trials.

5 of the 72 conditions linked to this drug’s targets have been checked against trial records so far. The rest are not ruled out — they are unchecked.

3 possible uses were rejected for pushing the wrong way. The target is linked to the condition, but the drug modulates it in the wrong direction.

Not yet used for these — 4

infantile-onset generalized dyskinesia with orofacia

Rejected — wrong way

It would be expected to worsen this condition. The genetic evidence indicates this condition requires the opposite modulation of the target. Shown rather than filtered so the direction check can be audited.

The condition
No description on file.
PDE10A · phosphodiesterase 10A
Plays a role in signal transduction by regulating the intracellular concentration of cyclic nucleotides (PubMed:10373451, PubMed:10393245, PubMed:16330539, PubMed:17389385, PubMed:27058447). Can hydrolyze both cAMP and cGMP, but has higher affinity for cAMP and is more efficient with cAMP as substrate (PubMed:10373451, PubMed:10393245, PubMed:17389385, PubMed:27058447). May play a critical role in regulating cAMP and cGMP levels in the striatum, a region of the brain that contributes to the control of movement and
Nobody has tried this
No registered trial of this drug in this condition.
What would kill it. Direction conflict, unless the variant has been assigned the wrong functional class — a known failure mode of consequence-based annotation.

striatal degeneration, autosomal dominant 2

Rejected — wrong way

It would be expected to worsen this condition. The genetic evidence indicates this condition requires the opposite modulation of the target. Shown rather than filtered so the direction check can be audited.

The condition
Any striatal degeneration, autosomal dominant in which the cause of the disease is a mutation in the PDE10A gene.
PDE10A · phosphodiesterase 10A
Plays a role in signal transduction by regulating the intracellular concentration of cyclic nucleotides (PubMed:10373451, PubMed:10393245, PubMed:16330539, PubMed:17389385, PubMed:27058447). Can hydrolyze both cAMP and cGMP, but has higher affinity for cAMP and is more efficient with cAMP as substrate (PubMed:10373451, PubMed:10393245, PubMed:17389385, PubMed:27058447). May play a critical role in regulating cAMP and cGMP levels in the striatum, a region of the brain that contributes to the control of movement and
Nobody has tried this
No registered trial of this drug in this condition.
What would kill it. Direction conflict, unless the variant has been assigned the wrong functional class — a known failure mode of consequence-based annotation.

Joubert syndrome with orofaciodigital defect

Rejected — wrong way

It would be expected to worsen this condition. The genetic evidence indicates this condition requires the opposite modulation of the target. Shown rather than filtered so the direction check can be audited.

The condition
Joubert syndrome with orofaciodigital defect (or oral-facial-digital syndrome type 6, OFD6) is a very rare subtype of Joubert syndrome and related disorders (JSRD, see this term) characterized by the neurological features of JS associated with orofacial anomalies and often polydactyly.
PDE6D · phosphodiesterase 6D
Promotes the release of prenylated target proteins from cellular membranes (PubMed:9712853). Modulates the activity of prenylated or palmitoylated Ras family members by regulating their subcellular location (PubMed:22002721, PubMed:23698361). Required for normal ciliary targeting of farnesylated target proteins, such as INPP5E (PubMed:24166846). Required for RAB28 localization to the cone cell outer segments in the retina (By similarity). Modulates the subcellular location of target proteins by acting as a GTP spec
Nobody has tried this
No registered trial of this drug in this condition.
What would kill it. Direction conflict, unless the variant has been assigned the wrong functional class — a known failure mode of consequence-based annotation.

psoriasis

Mechanism implies it

It could plausibly help.

The condition
An autoimmune condition characterized by red, well-delineated plaques with silvery scales that are usually on the extensor surfaces and scalp. They can occasionally present with these manifestations: pustules; erythema and scaling in intertriginous areas, and erythroderma, that are often distributed on extensor surfaces and scalp.
PDE4A · phosphodiesterase 4A
Hydrolyzes the second messenger 3',5'-cyclic AMP (cAMP), which is a key regulator of many important physiological processes. .
Nobody has tried this
No registered trial of this drug in this condition.
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach PDE4A in the relevant tissue at tolerated doses.
Already used for these — 1

Established practice, listed so the method can be checked against what is already known.

coronary artery disorder

Already in use

It is already used for this.

The condition
Narrowing of the coronary arteries due to fatty deposits inside the arterial walls. The diagnostic criteria may include documented history of any of the following: documented coronary artery stenosis greater than or equal to 50% (by cardiac catheterization or other modality of direct imaging of the coronary arteries); previous coronary artery bypass surgery (CABG); previous percutaneous coronary intervention (PCI); previous myocardial infarction. (ACC)
PDE5A · phosphodiesterase 5A
Plays a role in signal transduction by regulating the intracellular concentration of cyclic nucleotides. This phosphodiesterase catalyzes the specific hydrolysis of cGMP to 5'-GMP (PubMed:15489334, PubMed:9714779). Specifically regulates nitric-oxide- generated cGMP (PubMed:15489334). {ECO:0000269|PubMed:15489334, ECO:0000269|PubMed:9714779}.
In routine use
Established practice for this condition, not a new candidate.
NCT00129038 Modified-release Dipyridamole/Aspirin (2 · Ph 4 · 11 people
+14 more on ClinicalTrials.gov
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach PDE5A in the relevant tissue at tolerated doses.
05

Why nobody will fund it

8 companies make this across 17 approved products. With that many manufacturers the price has fallen to production cost. A company funding a trial could not recover it — competitors could market the same molecule for the new indication immediately, without contributing.

How abandoned it is63 / 100
0 to 100, calculated from manufacturer count, remaining patent or exclusivity, and whether any reformulation route to exclusivity is still open. 100 means no route to commercial return exists. The weights behind it are unsourced.
THE ONE WAY A COMPANY COULD STILL OWN IT
inhaledmodified-release

A new route or dosage form qualifies for a 505(b)(2) application, which carries three years of exclusivity for that formulation. It is the only remaining route to exclusivity on a generic molecule.

06

What it would cost to find out

Derived, not quoted. Events needed is 4(zα+zβ)²/ln(HR)²; enrolment is that divided by the event rate and follow-up. The 1/ln(HR)² term dominates: halving the detectable effect size roughly quadruples enrolment. derived

0.75
Lower = bigger effect = smaller trial
8.0%
2 yr
$32K
Unsourced placeholder
379
Events needed
3K
Patients
$93M
Trial cost
assumed
$10.82
Per person reached
assumed

Cost per person reached is the relevant metric for a non-commercial funder, since there is no revenue to set against the outlay.

07

Ask for ideas nobody has listed

Reasons from the functional groups and distribution above, excluding conditions already listed. Output is hypotheses for falsification, not findings. Not medical advice.

08

Who might pay for the trial

Trials of off-patent drugs are rarely funded by venture capital or pharma. They are paid for by government grants and disease foundations. Here is who has funded work on this molecule before, what federal mechanisms are open now, and which foundations fund trials in the disease areas it touches. measured

Federal grants that name this medicine
332 grants on NIH RePORTER
1ZIADA000493-20(NIDA · National Institute on Drug Abuse)Active
$2.9M (2025)
Functional and Pharmacological Significance of Receptor Heteromers in the CNS
PI: Ferre, Sergi · National Institute On Drug Abuse
1R21HD113856-01(NICHD · Eunice Kennedy Shriver NICHD)Concluded
$429K (2023)
NETs as therapeutic targets in obstetric APS
PI: Knight, Jason · University Of Michigan At Ann Arbor, Ann Arbor, MI · through 2023-12
1ZIADA000493-17(NIDA · National Institute on Drug Abuse)Concluded
$2.8M (2022)
Functional and Pharmacological Significance of Receptor Heteromers in the CNS
PI: Ferre, Sergi · National Institute On Drug Abuse
Open federal programmes that would fund this work

Open notices with an explicit mandate to fund work on approved or off-patent molecules.

RFA-CA-25-033National Institutes of HealthForecast — not open yet
Glioblastoma Therapeutics Network (GTN; U19 Clinical Trial Required)
RFA-FD-25-020Food and Drug Administrationcloses 05/16/2028
Reissue of RFA-FD-23-001- Clinical Studies of Orphan Products Addressing Unmet
FOR-FD-25-020Food and Drug AdministrationForecast — not open yet
Clinical Studies of Orphan Products Addressing Unmet Needs of Rare Diseases (R
FOR-FD-25-001Food and Drug AdministrationForecast — not open yet
Clinical Trials Addressing Unmet Needs of Rare Neurodegenerative Diseases (R01
RFA-TR-25-002National Institutes of Healthcloses 07/02/2027
Preclinical Proof of Concept Studies for Rare Diseases (R21 Clinical Trial Not
PAR-25-374National Institutes of Healthcloses 05/07/2028
Translational Bioinformatics and Experimental Approaches to Advance Drug Repos
HT942526PRCRPCTADefense Health Agency Contracting Activity -closes 10/05/2026
DoW Peer Reviewed Cancer, Clinical Trial Award
PAR-26-049National Institutes of HealthForecast — not open yet
Establishing Pediatric CNS Pharmacodynamic Measures as Tools to Enable Psychia
Showing 8 of 990 currently open under this category on Grants.gov, matched to the disease areas this drug touches. derived Browse all 990 on Grants.gov ↗
Funders beyond the federal system

Grants.gov lists US federal money. Many off-patent drug trials are supported by disease foundations and nonprofits. These are matched to the body systems this drug touches. assumed

Matched by disease area, not by molecule — a foundation appearing here funds work in a field this drug touches.
09

Who manufactures it

Companies holding an approved abbreviated application for this molecule in the United States, from the FDA Orange Book. Supply already exists at scale, so a trial would not need a manufacturing programme — but any of these could also be a partner, or an objector.

Barr Laboratories IncBarr Laboratories Llc (An Indirect Wholly Owned Sub Of Teva Pharmaceuticals Usa Inc)Chartwell Injectables Llc
8
Manufacturers
companies with their own approval
17
Approved products
distinct strengths and forms
2
Routes
injection, oral
1990
Oldest product still sold
approval year of the earliest product still on the market

Nothing on this page is medical advice. Candidate uses are unproven hypotheses derived from public data; established uses are listed for verification only. Figures carry their provenance inline — anything marked assumed or derived is not a measurement.

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