Sunitinib Malate

Other protein kinase inhibitors · given by oral · on the market since 2006

Leads

56.2M

People

Makers

How abandoned

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.

STICKS PERMANENTLY

Michael acceptor

What it does. Reacts with the sulfur groups on proteins, forming a permanent bond. The cell reads this as a chemical stress signal and switches on its whole antioxidant defence programme.

What it opens up. Any disease driven by oxidative stress or chronic inflammation, because the drug does not treat the disease so much as turn on the body's own repair response.

SETS HOW LONG IT LASTS

Aromatic fluorine

What it does. The liver attacks rings at predictable positions. Fluorine is small enough not to disturb the shape but strong enough that the attack fails, so the molecule survives longer.

What it opens up. Mainly a durability upgrade, but it also nudges the molecule into being slightly greasier, which helps it enter the brain.

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.

Intestinal lumen only

Poorly absorbed. Acts locally in the gut with minimal systemic exposure.

Easily

Skin

Crosses the stratum corneum. Viable as a topical.

Partly

Urinary tract

Cleared unchanged in urine. Local concentration exceeds plasma.

What it binds — and whether we can reach it · 8 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.

PDGFRB

Kinase · inhibitor

10.12

Engaged easily

KDR

Kinase · inhibitor

9.7

Engaged easily

KIT

Kinase · inhibitor

9.68

Engaged easily

FLT3

Kinase · inhibitor

9.66

Engaged easily

RET

Kinase · inhibitor

8.8

Engaged easily

CSF1R

Kinase · inhibitor

8.7

Engaged easily

FLT4

Kinase · inhibitor

7.77

Engaged

Target	Kind	Action	Affinity (pAct)	Can it be engaged?
PDGFRB	Kinase	inhibitor	10.12	Engaged easily
KDR	Kinase	inhibitor	9.7	Engaged easily
KIT	Kinase	inhibitor	9.68	Engaged easily
FLT3	Kinase	inhibitor	9.66	Engaged easily
RET	Kinase	inhibitor	8.8	Engaged easily
CSF1R	Kinase	inhibitor	8.7	Engaged easily
FLT4	Kinase	inhibitor	7.77	Engaged

This molecule builds up inside cells far above blood levels. Local concentration therefore exceeds plasma, so targets that look unreachable on a plasma reading may still be engaged. assumed

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 173 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 — 4

medullary thyroid gland carcinoma

Tried in people

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

The condition

A neuroendocrine carcinoma arising from the C-cells of the thyroid gland. It is closely associated with multiple endocrine neoplasia syndromes. Approximately 10% to 20% of medullary thyroid carcinomas are familial. Patients usually present with a thyroid nodule that is painless and firm. In the majority of cases nodal involvement is present at diagnosis. Surgery is the preferred treatment for both primary lesions and recurrences. This carcinoma is generally not very sensitive to radiation and almost unresponsive to

RET · ret proto-oncogene

Receptor tyrosine-protein kinase involved in numerous cellular mechanisms including cell proliferation, neuronal navigation, cell migration, and cell differentiation in response to glia cell line- derived growth family factors (GDNF, NRTN, ARTN, PSPN and GDF15) (PubMed:20064382, PubMed:20616503, PubMed:20702524, PubMed:21357690, PubMed:21454698, PubMed:24560924, PubMed:28846097, PubMed:28846099, PubMed:28953886, PubMed:31118272). In contrast to most receptor tyrosine kinases, RET requires not only its cognate ligan

Open Targets scores each kind of evidence from 0.00 to 1.00 for this exact pairing — RET and medullary thyroid gland carcinoma. The score reflects how much evidence of that kind exists and how consistent it is. It is not a probability that the drug works. Rows are ordered by how much each kind counts toward the evidence figure used in the ranking, not by its raw score, because the two disagree: literature co-occurrence saturates near 1.00 on almost any well-studied pair, while genetic association rarely exceeds 0.70 even when causal.

Genetic association0.94 / 1.00

Inherited variants in this gene alter disease risk in human populations. The datatype most predictive of later clinical success.55% of evidence score

Somatic mutation0.61 / 1.00

This gene is recurrently mutated in this tumour type.15% of evidence score

Animal model0.35 / 1.00

Altering this gene in animals reproduces or relieves the disease phenotype.15% of evidence score

Curated genetic literature0.80 / 1.00

Gene–disease links curated from published genetic studies.5% of evidence score

Literature co-occurrence0.99 / 1.00

Gene and condition appear together in published text. Reflects publication volume, not causal evidence.2% of evidence score

Clinical0.94 / 1.00

Derived from clinical or trial records.not counted

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.

NCT00381641 Sunitinib Malate in Treating Patients Wi · Ph 2 · 63 people

+2 more on ClinicalTrials.gov

What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach RET in the relevant tissue at tolerated doses.

multiple endocrine neoplasia type 2A

Wide open

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

The condition

An autosomal dominant tumor predisposition disorder caused by pathogenic variants in the RET gene, characterized by an increased risk of medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism.

RET · ret proto-oncogene

Open Targets scores each kind of evidence from 0.00 to 1.00 for this exact pairing — RET and multiple endocrine neoplasia type 2A. The score reflects how much evidence of that kind exists and how consistent it is. It is not a probability that the drug works. Rows are ordered by how much each kind counts toward the evidence figure used in the ranking, not by its raw score, because the two disagree: literature co-occurrence saturates near 1.00 on almost any well-studied pair, while genetic association rarely exceeds 0.70 even when causal.

Genetic association0.94 / 1.00

Inherited variants in this gene alter disease risk in human populations. The datatype most predictive of later clinical success.55% of evidence score

Curated genetic literature0.84 / 1.00

Gene–disease links curated from published genetic studies.5% of evidence score

Literature co-occurrence0.46 / 1.00

Gene and condition appear together in published text. Reflects publication volume, not causal evidence.2% of evidence score

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 RET in the relevant tissue at tolerated doses.

leukoencephalopathy, diffuse hereditary, with sphero

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

A rare autosomal dominant disease characterized by a complex phenotype including progressive dementia, apraxia, apathy, impaired balance, parkinsonism, spasticity and epilepsy.

CSF1R · colony stimulating factor 1 receptor

Tyrosine-protein kinase that acts as a cell-surface receptor for CSF1 and IL34 and plays an essential role in the regulation of survival, proliferation and differentiation of hematopoietic precursor cells, especially mononuclear phagocytes, such as macrophages and monocytes. Promotes the release of pro-inflammatory chemokines in response to IL34 and CSF1, and thereby plays an important role in innate immunity and in inflammatory processes. Plays an important role in the regulation of osteoclast proliferation and di

Open Targets scores each kind of evidence from 0.00 to 1.00 for this exact pairing — CSF1R and leukoencephalopathy, diffuse hereditary, with sphero. The score reflects how much evidence of that kind exists and how consistent it is. It is not a probability that the drug works. Rows are ordered by how much each kind counts toward the evidence figure used in the ranking, not by its raw score, because the two disagree: literature co-occurrence saturates near 1.00 on almost any well-studied pair, while genetic association rarely exceeds 0.70 even when causal.

Genetic association0.93 / 1.00

Inherited variants in this gene alter disease risk in human populations. The datatype most predictive of later clinical success.55% of evidence score

Animal model0.43 / 1.00

Altering this gene in animals reproduces or relieves the disease phenotype.15% of evidence score

Curated genetic literature0.84 / 1.00

Gene–disease links curated from published genetic studies.5% of evidence score

Literature co-occurrence0.04 / 1.00

Gene and condition appear together in published text. Reflects publication volume, not causal evidence.2% of evidence score

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.

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.

FLT3 · fms related receptor tyrosine kinase 3

Tyrosine-protein kinase that acts as a cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation o

Open Targets scores each kind of evidence from 0.00 to 1.00 for this exact pairing — FLT3 and acute myeloid leukemia. The score reflects how much evidence of that kind exists and how consistent it is. It is not a probability that the drug works. Rows are ordered by how much each kind counts toward the evidence figure used in the ranking, not by its raw score, because the two disagree: literature co-occurrence saturates near 1.00 on almost any well-studied pair, while genetic association rarely exceeds 0.70 even when causal.

Genetic association0.55 / 1.00

Inherited variants in this gene alter disease risk in human populations. The datatype most predictive of later clinical success.55% of evidence score

Somatic mutation0.85 / 1.00

This gene is recurrently mutated in this tumour type.15% of evidence score

Animal model0.62 / 1.00

Altering this gene in animals reproduces or relieves the disease phenotype.15% of evidence score

Pathway0.84 / 1.00

The gene sits in a pathway with established disruption in this condition.8% of evidence score

Curated genetic literature0.30 / 1.00

Gene–disease links curated from published genetic studies.5% of evidence score

Literature co-occurrence1.00 / 1.00

Gene and condition appear together in published text. Reflects publication volume, not causal evidence.2% of evidence score

Clinical0.97 / 1.00

Derived from clinical or trial records.not counted

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.

NCT01620216 Targeted Therapy in Treating Patients Wi · Ph 2 · 12 people

+6 more on ClinicalTrials.gov

What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach FLT3 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.

gastrointestinal stromal tumor

Already in use

It is already used for this.

The condition

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm of the gastrointestinal (GI) tract, typically presenting in adults over the age of 40 (mean age 63), and only rarely in children, in various regions of the GI tract, most commonly the stomach or small intestine but also less commonly in the esophagus, appendix, rectum and colon. GISTs can be asymptomatic or present with various non-specific signs, depending on the location and size of tumor, such as loss of appetite, anemia, weight loss,

KIT · KIT proto-oncogene, receptor tyrosine kinase

Tyrosine-protein kinase that acts as a cell-surface receptor for the cytokine KITLG/SCF and plays an essential role in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and in melanogenesis. In response to KITLG/SCF binding, KIT can activate several signaling pathways. Phosphorylates PIK3R1, PLCG1, SH2B2/APS and CBL. Activates the AKT1 signaling pathway by phosphorylation of PIK3R1, the regulatory subunit of phospha

Open Targets scores each kind of evidence from 0.00 to 1.00 for this exact pairing — KIT and gastrointestinal stromal tumor. The score reflects how much evidence of that kind exists and how consistent it is. It is not a probability that the drug works. Rows are ordered by how much each kind counts toward the evidence figure used in the ranking, not by its raw score, because the two disagree: literature co-occurrence saturates near 1.00 on almost any well-studied pair, while genetic association rarely exceeds 0.70 even when causal.

Genetic association0.91 / 1.00

Inherited variants in this gene alter disease risk in human populations. The datatype most predictive of later clinical success.55% of evidence score

Somatic mutation0.78 / 1.00

This gene is recurrently mutated in this tumour type.15% of evidence score

Animal model0.48 / 1.00

Altering this gene in animals reproduces or relieves the disease phenotype.15% of evidence score

Pathway0.90 / 1.00

The gene sits in a pathway with established disruption in this condition.8% of evidence score

Curated genetic literature0.82 / 1.00

Gene–disease links curated from published genetic studies.5% of evidence score

Literature co-occurrence0.99 / 1.00

Gene and condition appear together in published text. Reflects publication volume, not causal evidence.2% of evidence score

Clinical0.98 / 1.00

Derived from clinical or trial records.not counted

In routine use

Established practice for this condition, not a new candidate.

NCT00793871 Safety And Efficacy Study Of Sunitinib M · Ph 4 · 60 people

+14 more on ClinicalTrials.gov

What would kill it. A null trial, or pharmacokinetic data showing the drug does not reach KIT in the relevant tissue at tolerated doses.

Why nobody will fund it

8 companies make this across 32 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 is48 / 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

topicalinjectableinhaledmodified-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.

What it would cost to find out

Derived, not quoted. Events needed is 4(z_α+z_β)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

Effect sought (hazard ratio)0.75

Lower = bigger effect = smaller trial

How often the event happens per year8.0%

Follow-up2 yr

Cost per patient$32K

Unsourced placeholder

379

Events needed

Patients

$93M

Trial cost

assumed

$4.72

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.

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.

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

322 grants on NIH RePORTER

5R00HL166693-04(NHLBI · National Heart, Lung & Blood Institute)Active

$249K (2026)

Elucidating anti-angiogenic tyrosine kinase inhibitor-induced vascular dysfunction

PI: Shen, Mengcheng · Washington University, Saint Louis, MO · through 2028-06

View on NIH RePORTER ↗Apply to same mechanism (PA-20-188) ↗

5R01CA295558-02(NCI · National Cancer Institute)Active

$600K (2026)

Generating Synthetic Lethality in Glioblastoma with a First-In-Class Non-Muscle Myosin II Inhibitor

PI: Rosenfeld, Steven S · Mayo Clinic Jacksonville, Jacksonville, FL · through 2029-12

View on NIH RePORTER ↗Apply to same mechanism (PA-20-185) ↗

5R01HL173315-02(NHLBI · National Heart, Lung & Blood Institute)Active

$688K (2026)

Molecular mechanisms of translational control in sunitinib-induced vascular dysfunction

PI: Ong, Sang Ging · University Of Illinois At Chicago, Chicago, IL · through 2029-11

View on NIH RePORTER ↗Apply to same mechanism (PA-20-185) ↗

See all 322 projects on NIH RePORTER →

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)

Grants.gov (RFA-CA-25-033) ↗Direct listing ↗Who already holds this grant ↗

RFA-FD-25-020Food and Drug Administrationcloses 05/16/2028

Reissue of RFA-FD-23-001- Clinical Studies of Orphan Products Addressing Unmet

Read announcement ↗Grants.gov (RFA-FD-25-020) ↗Direct listing ↗Who already holds this grant ↗

FOR-FD-25-020Food and Drug AdministrationForecast — not open yet

Clinical Studies of Orphan Products Addressing Unmet Needs of Rare Diseases (R

Grants.gov (FOR-FD-25-020) ↗Direct listing ↗Who already holds this grant ↗

FOR-FD-25-001Food and Drug AdministrationForecast — not open yet

Clinical Trials Addressing Unmet Needs of Rare Neurodegenerative Diseases (R01

Grants.gov (FOR-FD-25-001) ↗Direct listing ↗Who already holds this grant ↗

RFA-TR-25-002National Institutes of Healthcloses 07/02/2027

Preclinical Proof of Concept Studies for Rare Diseases (R21 Clinical Trial Not

Read announcement ↗Grants.gov (RFA-TR-25-002) ↗Direct listing ↗Who already holds this grant ↗

PAR-25-374National Institutes of Healthcloses 05/07/2028

Translational Bioinformatics and Experimental Approaches to Advance Drug Repos

Read announcement ↗Grants.gov (PAR-25-374) ↗Direct listing ↗Who already holds this grant ↗

HT942526PRCRPCTADefense Health Agency Contracting Activity -closes 10/05/2026

DoW Peer Reviewed Cancer, Clinical Trial Award

Grants.gov (HT942526PRCRPCTA) ↗Direct listing ↗Who already holds this grant ↗

PAR-26-049National Institutes of HealthForecast — not open yet

Establishing Pediatric CNS Pharmacodynamic Measures as Tools to Enable Psychia

Grants.gov (PAR-26-049) ↗Direct listing ↗Who already holds this grant ↗

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.

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.

Dr Reddys Laboratories LtdEugia Pharma Specialities LtdFosun Wanbang (Jiangsu) Pharmaceutical Group Co Ltd

Manufacturers

companies with their own approval

Approved products

distinct strengths and forms

Routes

oral

2006

Oldest product still sold

approval year of the earliest product still on the market

ALSO SOLD AS

SUTENT

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.

← Back to the full ledger

What it's made of

Basic amine

Michael acceptor

Aromatic fluorine

Where it can get to

What it binds — and whether we can reach it · 8 of 7 reachable

New uses, and who is already trying them

medullary thyroid gland carcinoma

multiple endocrine neoplasia type 2A

leukoencephalopathy, diffuse hereditary, with sphero

acute myeloid leukemia

gastrointestinal stromal tumor

Why nobody will fund it

What it would cost to find out

Ask for ideas nobody has listed

Who might pay for the trial

Who manufactures it

Closely related medicines