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Sotalol Hydrochloride

Beta blocking agents, non-selective · given by intravenous, oral · on the market since 1992

5
Leads
23.3M
People
7
Makers
13
How abandoned
01

What it's made of

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

SETS WHERE IT GOES

Basic amine

What it does. Neutral enough to slip through membranes, then becomes charged inside the acidic compartments of the cell and gets trapped there. Concentrations inside cells can reach many times the blood level.

What it opens up. Diseases of the cell's internal recycling compartments, and a common reason a drug accumulates in lung, liver, and eye tissue far beyond what the blood level suggests.

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

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

What it binds — and whether we can reach it · 2 of 3 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.
ADRB2
GPCR · antagonist
6.9
Just reachable
ADRB1
GPCR · antagonist
6.1
Just reachable
KCNH2
Ion channel · blocker
4
Not reachable

This molecule builds up inside cells far above blood levels, 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 78 conditions linked to this drug’s targets have been checked against trial records so far. The rest are not ruled out — they are unchecked.

1 possible use was 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 — 3

Romano-Ward syndrome

Wide open

It acts on a target linked to this disease; untested, and the direction of effect is unverified.

The condition
No description on file.
KCNH2 · potassium voltage-gated channel subfamily H member 2
Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel (PubMed:10219239, PubMed:10753933, PubMed:10790218, PubMed:10837251, PubMed:11997281, PubMed:12063277, PubMed:18559421, PubMed:22314138, PubMed:22359612, PubMed:26363003, PubMed:27916661, PubMed:9230439, PubMed:9351446, PubMed:9765245). Channel properties are modulated by cAMP and subunit assembly (PubMed:10837251). Characterized by unusual gating kinetics by producing relatively small outward currents during membrane depolarization
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 KCNH2 in the relevant tissue at tolerated doses.

Familial short QT syndrome

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.
KCNH2 · potassium voltage-gated channel subfamily H member 2
Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel (PubMed:10219239, PubMed:10753933, PubMed:10790218, PubMed:10837251, PubMed:11997281, PubMed:12063277, PubMed:18559421, PubMed:22314138, PubMed:22359612, PubMed:26363003, PubMed:27916661, PubMed:9230439, PubMed:9351446, PubMed:9765245). Channel properties are modulated by cAMP and subunit assembly (PubMed:10837251). Characterized by unusual gating kinetics by producing relatively small outward currents during membrane depolarization
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.

hypertensive disorder

Animal models only

It reduces disease in animal models; untested in humans.

The condition
Persistently high systemic arterial blood pressure. Based on multiple readings (blood pressure determination), hypertension is currently defined as when systolic pressure is consistently greater than 140 mm Hg or when diastolic pressure is consistently 90 mm Hg or more.
ADRB1 · adrenoceptor beta 1
G protein-coupled receptor for catecholamines that couples to G(s) proteins to activate adenylate cyclase and cAMP-dependent pathway (PubMed:10212248, PubMed:12391161, PubMed:15358775). Binds epinephrine and norepinephrine with approximately equal affinity (PubMed:33093660). Mediates the activation of Ras via binding with cAMP-dependent RAPGEF2 (PubMed:12391161). As part of the sympathetic nervous system, plays a role in the physiologic regulation of cardiac functions such as stimulation of cardiomyocyte contractio
Phase 1 only
Safety and dose-finding studies exist. No efficacy data.
NCT05794997 Data Analysis for Drug Repurposing for E · NA · 817337 people
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach ADRB1 in the relevant tissue at tolerated doses.
Already used for these — 2

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

atrial fibrillation

Already in use

It is already used for this.

The condition
A disorder characterized by an electrocardiographic finding of a supraventricular arrhythmia characterized by the replacement of consistent P waves by rapid oscillations or fibrillatory waves that vary in size, shape and timing and are accompanied by an irregular ventricular response. (CDISC)
KCNH2 · potassium voltage-gated channel subfamily H member 2
Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel (PubMed:10219239, PubMed:10753933, PubMed:10790218, PubMed:10837251, PubMed:11997281, PubMed:12063277, PubMed:18559421, PubMed:22314138, PubMed:22359612, PubMed:26363003, PubMed:27916661, PubMed:9230439, PubMed:9351446, PubMed:9765245). Channel properties are modulated by cAMP and subunit assembly (PubMed:10837251). Characterized by unusual gating kinetics by producing relatively small outward currents during membrane depolarization
In routine use
Established practice for this condition, not a new candidate.
NCT01477983 Kansai Plus Atrial Fibrillation Trial · Ph 4 · 2113 people
+14 more on ClinicalTrials.gov
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach KCNH2 in the relevant tissue at tolerated doses.

cardiac arrhythmia

Already in use

It is already used for this.

The condition
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
KCNH2 · potassium voltage-gated channel subfamily H member 2
Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel (PubMed:10219239, PubMed:10753933, PubMed:10790218, PubMed:10837251, PubMed:11997281, PubMed:12063277, PubMed:18559421, PubMed:22314138, PubMed:22359612, PubMed:26363003, PubMed:27916661, PubMed:9230439, PubMed:9351446, PubMed:9765245). Channel properties are modulated by cAMP and subunit assembly (PubMed:10837251). Characterized by unusual gating kinetics by producing relatively small outward currents during membrane depolarization
In routine use
Established practice for this condition, not a new candidate.
NCT01477983 Kansai Plus Atrial Fibrillation Trial · Ph 4 · 2113 people
+14 more on ClinicalTrials.gov
What would kill it. Direction conflict, unless the variant has been assigned the wrong functional class — a known failure mode of consequence-based annotation.
05

Why nobody will fund it

7 companies make this across 31 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 is13 / 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
topicalinhaledmodified-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
$11.37
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
86 grants on NIH RePORTER
1UG3DA064414-01(NIDA · National Institute on Drug Abuse)Active
$2.3M (2026)
Safety and preliminary efficacy of ibogaine as a treatment for opioid use disorder
PI: Suzuki, Joji · Brigham And Women'S Hospital, Boston, MA · through 2028-05
1F32HL182152-01(NHLBI · National Heart, Lung & Blood Institute)Active
$80K (2025)
Toward the Precision Diagnosis and Prevention of Acquired and Congenital Long QT Arrhythmias
PI: Liu, Michael Bon-Hao · Stanford University, Stanford, CA · through 2028-09
1R43HL174305-01(NHLBI · National Heart, Lung & Blood Institute)Concluded
$295K (2024)
A novel, smartwatch-enabled, automated mobile heart rhythm analysis technology to start antiarrhythmic medications safely at home
PI: Navara, Rachita · Safebeat Rx Inc., Carson, CA · through 2026-02
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.

Aiping Pharmaceutical IncApotex IncAurobindo Pharma Usa Inc
7
Manufacturers
companies with their own approval
31
Approved products
distinct strengths and forms
2
Routes
intravenous, oral
1992
Oldest product still sold
approval year of the earliest product still on the market
ALSO SOLD AS
BETAPACEBETAPACE AFSORINE

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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