ArticleCancer chemotherapy and pharmacology2017
Absorption, metabolism, and excretion of [
Article in Cancer chemotherapy and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- Mapping the ATP-Binding Pockets of FLT3 and TAK1: A Structural Basis for Dual Inhibition by FLT3-Targeted Therapies.ACS chemical biology · 2026Article
- Cellular Context Influences Kinase Inhibitor Selectivity.Journal of medicinal chemistry · 2026Article
- Cellular Selectivity Analyses Reveal Distinguishing Profiles for Type II Kinase Inhibitors.bioRxiv : the preprint server for biology · 2025Article
- The Adverse Impact of Tyrosine Kinase Inhibitors on Wound Healing and Repair.International wound journal · 2025Review
- Allosteric coupling asymmetry mediates paradoxical activation of BRAF by type II inhibitors.eLife · 2024Article
- Article
- Population Pharmacokinetics of Ponatinib in Healthy Adult Volunteers and Patients With Hematologic Malignancies and Model-Informed Dose Selection for Pediatric Development.Journal of clinical pharmacology · 2022Article
- Transport and metabolism of tyrosine kinase inhibitors associated with chronic myeloid leukemia therapy: a review.Molecular and cellular biochemistry · 2022Review
- Ponatinib and other CML Tyrosine Kinase Inhibitors in Thrombosis.International journal of molecular sciences · 2020Review
- Inhibitors of BRAF dimers using an allosteric site.Nature communications · 2020Article
- Pharmacology of tyrosine kinase inhibitors in chronic myeloid leukemia; a clinician's perspective.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Review
- Utilizing Stimulated Raman Scattering Microscopy To Study Intracellular Distribution of Label-Free Ponatinib in Live Cells.Journal of medicinal chemistry · 2020Article
- A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein.Communications biology · 2020Article
- Insights into the optimal use of ponatinib in patients with chronic phase chronic myeloid leukaemia.Therapeutic advances in hematology · 2019Review
- Ponatinib (AP24534) inhibits MEKK3-KLF signaling and prevents formation and progression of cerebral cavernous malformations.Science advances · 2018Article
- Identification and characterization of prescription drugs that change levels of 7-dehydrocholesterol and desmosterol.Journal of lipid research · 2018Article
- Alkynylnicotinamide-Based Compounds as ABL1 Inhibitors with Potent Activities against Drug-Resistant CML Harboring ABL1(T315I) Mutant Kinase.ChemMedChem · 2018Article
- Ponatinib Activates an Inflammatory Response in Endothelial Cells via ERK5 SUMOylation.Frontiers in cardiovascular medicine · 2018Article
- Mutations in the breakpoint cluster region-Abelson murine leukemia 1 gene in Brazilian patients with chronic myeloid leukemia.Hematology, transfusion and cell therapyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePonatinib is a novel tyrosine kinase inhibitor (TKI) specifically designed to inhibit native and mutated BCR-ABL. In the United States, ponatinib has received accelerated approval for adults with T315I-positive chronic myeloid leukemia (CML) or T315I (gatekeeper mutation)-positive, Philadelphia chromosome-positive, acute lymphoblastic leukemia (Ph + ALL), and patients with CML or Ph + ALL for whom no other TKI therapy is indicated. The objective of this phase 1, mass balance study was to evaluate the absorption, metabolism, and excretion of [
methodsA single 45-mg [
results86.6 and 5.4% of the dose was recovered in feces and urine, respectively, during days 0-14 postdose. Median time to maximal plasma radioactivity was 5 h and mean terminal elimination half-life of radioactivity was 66.4 h. Ponatinib and its inactive carboxylic acid metabolite M14, the two major circulating radioactive components, accounted for 25.5 and 14.9% of the radioactivity in 0-24 h pooled plasma, with elimination half-lives of 27.4 and 33.7 h, respectively. Major metabolites in urine were M14 and its glucuronides, which, together with other M14-derived metabolites, represented 4.4% of the dose; ponatinib was not detected in urine. In feces, major radioactive components were ponatinib, M31 (hydroxylation), M42 (N-demethylation), and four methylated products accounting for 20.5, 17.7, 8.3, and 8.4% of the radioactive dose, respectively.
conclusionsPonatinib was readily absorbed in humans, metabolized through multiple pathways and was eliminated mostly in feces.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.