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Mitoxantrone Hydrochloride

Anthracyclines and related substances · given by injection · on the market since 2006

5
Leads
18.0M
People
4
Makers
42
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.

SETS HOW LONG IT LASTS

Phenol

What it does. The liver's favourite attachment point. It tags this group and flushes the molecule out, often within an hour.

What it opens up. Usually shortens the drug's life. Blocking or masking this position is the standard way to make a compound last longer.

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

Barely
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.
Easily
Urinary tract
Cleared unchanged in urine. Local concentration exceeds plasma.
03

What it binds — and whether we can reach it

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.
TOP2A
Enzyme · inhibitor
5.96
Out of reach

This molecule builds up inside cells far above blood levels, sits in the gut at high concentration, concentrates in urine. Local concentration therefore exceeds plasma, so targets that look unreachable on a plasma reading may still be engaged. assumed

Cytotoxic. Targets core cell-division machinery. Use is limited to conditions severe enough to justify that toxicity; risk-benefit inverts in chronic benign disease.

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

Not yet used for these — 5

neoplasm

Tried in people

It showed an effect in a human trial that was not followed up.

The condition
A benign or malignant tissue growth resulting from uncontrolled cell proliferation. Benign neoplastic cells resemble normal cells without exhibiting significant cytologic atypia, while malignant cells exhibit overt signs such as dysplastic features, atypical mitotic figures, necrosis, nuclear pleomorphism, and anaplasia. Representative examples of benign neoplasms include papillomas, cystadenomas, and lipomas; malignant neoplasms include carcinomas, sarcomas, lymphomas, and leukemias.
TOP2A · DNA topoisomerase II alpha
Key decatenating enzyme that alters DNA topology by binding to two double-stranded DNA molecules, generating a double-stranded break in one of the strands, passing the intact strand through the broken strand, and religating the broken strand (PubMed:17567603, PubMed:18790802, PubMed:22013166, PubMed:22323612, PubMed:27754753). May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity). {ECO:0000250|UniProtKB:Q01320, ECO:0000269|PubMed:17567603, ECO:0000269|PubMed:18790802,
Phase 3 has run
A Phase 3 trial exists. Read its result before anything else.
NCT00002766 Comparison of Two Combination Chemothera · Ph 3 · 170 people
+14 more on ClinicalTrials.gov
What would kill it. A null result in the completed Phase 3.

breast cancer

Tried in people

It showed an effect in a human trial that was not followed up.

The condition
A primary or metastatic malignant neoplasm involving the breast. The vast majority of cases are carcinomas arising from the breast parenchyma or the nipple. Malignant breast neoplasms occur more frequently in females than in males.
TOP2A · DNA topoisomerase II alpha
Key decatenating enzyme that alters DNA topology by binding to two double-stranded DNA molecules, generating a double-stranded break in one of the strands, passing the intact strand through the broken strand, and religating the broken strand (PubMed:17567603, PubMed:18790802, PubMed:22013166, PubMed:22323612, PubMed:27754753). May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity). {ECO:0000250|UniProtKB:Q01320, ECO:0000269|PubMed:17567603, ECO:0000269|PubMed:18790802,
Phase 3 has run
A Phase 3 trial exists. Read its result before anything else.
NCT00003893 Adjuvant Chemotherapy Plus Radiation The · Ph 3 · 2250 people
+11 more on ClinicalTrials.gov
What would kill it. A null result in the completed Phase 3.

acute myeloid leukemia

Tried in people

It showed an effect in a human trial that was not followed up.

The condition
Acute myeloid leukemia (AML) is a group of neoplasms arising from precursor cells committed to the myeloid cell-line differentiation. All of them are characterized by clonal expansion of myeloid blasts. AML manifests by fever, pallor, anemia, hemorrhages and recurrent infections.
TOP2A · DNA topoisomerase II alpha
Key decatenating enzyme that alters DNA topology by binding to two double-stranded DNA molecules, generating a double-stranded break in one of the strands, passing the intact strand through the broken strand, and religating the broken strand (PubMed:17567603, PubMed:18790802, PubMed:22013166, PubMed:22323612, PubMed:27754753). May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity). {ECO:0000250|UniProtKB:Q01320, ECO:0000269|PubMed:17567603, ECO:0000269|PubMed:18790802,
Phase 3 has run
A Phase 3 trial exists. Read its result before anything else.
NCT03250338 Study Investigating the Efficacy of Cren · Ph 3 · 106 people
+14 more on ClinicalTrials.gov
What would kill it. A null result in the completed Phase 3.

plasma cell myeloma

Tried in people

It showed an effect in a human trial that was not followed up.

The condition
A bone marrow-based plasma cell neoplasm characterized by a serum monoclonal protein and skeletal destruction with osteolytic lesions, pathological fractures, bone pain, hypercalcemia, and anemia. Clinical variants include non-secretory myeloma, smoldering myeloma, indolent myeloma, and plasma cell leukemia. (WHO, 2001)
TOP2A · DNA topoisomerase II alpha
Key decatenating enzyme that alters DNA topology by binding to two double-stranded DNA molecules, generating a double-stranded break in one of the strands, passing the intact strand through the broken strand, and religating the broken strand (PubMed:17567603, PubMed:18790802, PubMed:22013166, PubMed:22323612, PubMed:27754753). May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity). {ECO:0000250|UniProtKB:Q01320, ECO:0000269|PubMed:17567603, ECO:0000269|PubMed:18790802,
Phase 2 done, then stopped
A Phase 2 trial finished and was not followed by Phase 3. Dosing and safety in this population are already established.
NCT00100477 Use of Topotecan in Patients With Refrac · Ph 2 · 10 people
+4 more on ClinicalTrials.gov
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach TOP2A in the relevant tissue at tolerated doses.

small cell lung carcinoma

Tried in people

It showed an effect in a human trial that was not followed up.

The condition
Small cell lung cancer (SCLC) is a highly aggressive malignant neoplasm, accounting for 10-15% of lung cancer cases, characterized byrapid growth, and early metastasis. SCLC usually manifests as a large hilar mass with bulky mediastinal lymphadenopathy presenting clinically with chest pain, persistent cough, dyspnea, wheezing, hoarseness, hemoptysis, loss of appetite, weight loss, and neurological and endocrine paraneoplastic syndromes. SCLC is primarily reported in elderly people with a history of long-term tobacc
TOP2A · DNA topoisomerase II alpha
Key decatenating enzyme that alters DNA topology by binding to two double-stranded DNA molecules, generating a double-stranded break in one of the strands, passing the intact strand through the broken strand, and religating the broken strand (PubMed:17567603, PubMed:18790802, PubMed:22013166, PubMed:22323612, PubMed:27754753). May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity). {ECO:0000250|UniProtKB:Q01320, ECO:0000269|PubMed:17567603, ECO:0000269|PubMed:18790802,
Phase 2 done, then stopped
A Phase 2 trial finished and was not followed by Phase 3. Dosing and safety in this population are already established.
NCT04352413 A Study of PLM60 in Subjects With Relaps · Ph 2 · 45 people
What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach TOP2A in the relevant tissue at tolerated doses.
05

Why nobody will fund it

4 companies make this across 12 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 is42 / 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
$14.70
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
287 grants on NIH RePORTER
5R01GM126363-08(NIGMS · National Institute of General Medical Sciences)Active
$356K (2025)
Mechanistic Studies of Type II Topoisomerases and Topoisomerase-Targeted Agents
PI: Osheroff, Neil · Vanderbilt University, Nashville, TN · through 2026-11
5R01CA248064-05(NCI · National Cancer Institute)Concluded
$364K (2025)
Cause and therapeutic impact of DNA-protein crosslink repair defect in myeloid leukemias
PI: Kaufmann, Scott H · Mayo Clinic Rochester, Rochester, MN · through 2026-06
5R01CA292071-02(NCI · National Cancer Institute)Concluded
$437K (2025)
Targeting mitochondrial calcium to eradicate leukemia-initiating cells
PI: Jordan, Craig T. · University Of Colorado Denver, Aurora, CO · through 2026-07
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.

Fresenius Kabi Usa LlcHikma Pharmaceuticals Usa IncHospira Worldwide, Inc
4
Manufacturers
companies with their own approval
12
Approved products
distinct strengths and forms
1
Routes
injection
2006
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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