Evidence map›Paper›PMID 38710951›Full record

Trial reportNature medicine2024

Pemigatinib in previously treated solid tumors with activating FGFR1-FGFR3 alterations: phase 2 FIGHT-207 basket trial.

Jordi Rodón, Silvia Damian, Muhammad Furqan, Jesús García-Donas, Hiroo Imai, Antoine Italiano, Iben Spanggaard, Makoto Ueno, Tomoya Yokota, Maria Luisa Veronese and 5 more

Erratum issued Registry-linked trialAbstract readClinical Trial, Phase II
In one paragraph

Trial report in Nature medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT03822117 (A Phase 2, Open-Label, Single-Arm, Multicenter Study to Evaluate the Efficacy and Safety of Pemigatinib in Participants With Previously Treated Locally Advanced/Metastatic or Surgically Unresectable Solid Tumor Malignancies Harboring Activating FGFR Mutations or Translocations), which is not on this map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

NCT03822117 phase2terminatednot on this map

A Phase 2, Open-Label, Single-Arm, Multicenter Study to Evaluate the Efficacy and Safety of Pemigatinib in Participants With Previously Treated Locally Advanced/Metastatic or Surgically Unresectable Solid Tumor Malignancies Harboring Activating FGFR Mutations or Translocations (FIGHT-207)

TypeinterventionalSponsorIncyte CorporationRan2019 to 2022Enrolled111ConditionsSolid Tumor MalignancyArmsPemigatinib
3 · Its place in the literature

Who cites it

44 citing papers in PubMed.

  1. Trial
  2. Recurrent Resistance Mutations to Lirafugratinib Inform Treatment Sequencing in FGFR2-Driven Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
  3. Erdafitinib in Patients with FGFR-Altered Advanced or Metastatic Cholangiocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
  4. Trial
  5. Article
  6. Review
  7. Advances in the management of pediatric low-grade glioma.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Recent Advances in Targeted Therapies for Adult Gliomas.Current neurology and neuroscience reports · 2026
    Review
  12. The conserved fibroblast growth factor receptor-based signaling is required for dendrite regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  13. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. FGFR1 fusions in genomically and epigenetically bona fide glioblastoma, IDH-wildtype.Journal of neuropathology and experimental neurology · 2026
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Jordi RodónThe University of Texas MD Anderson Cancer Center, Houston, TX, USA. jrodon@mdanderson.org.ORCID 0000-0001-6467-3632
Silvia DamianFondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.ORCID 0000-0001-9560-1092
Muhammad FurqanUniversity of Iowa, Iowa City, IA, USA.
Jesús García-DonasCentro Integral Oncologico Clara Campal, Madrid, Spain.ORCID 0000-0001-7731-3601
Hiroo ImaiTohoku University Hospital, Sendai-Shi, Japan.
Antoine ItalianoInstitut Bergonié, Bordeaux, France.ORCID 0000-0002-8540-5351
Iben SpanggaardRigshospitalet Copenhagen University Hospital, Copenhagen, Denmark.ORCID 0000-0001-5925-2630
Makoto UenoKanagawa Cancer Center, Yokohama, Japan.
Tomoya YokotaShizuoka Cancer Center, Shizuoka, Japan.ORCID 0000-0001-7327-7949
Maria Luisa VeroneseIncyte International Biosciences Sàrl, Morges, Switzerland.
Natalia OliveiraIncyte International Biosciences Sàrl, Morges, Switzerland.
Xin LiIncyte Corporation, Wilmington, DE, USA.
Aidan GilmartinIncyte Corporation, Wilmington, DE, USA.
Michael SchafferIncyte Corporation, Wilmington, DE, USA.ORCID 0000-0003-1381-0275
Lipika GoyalMass General Cancer Center, Harvard Medical School, Boston, MA, USA. lgoyal@stanford.edu.ORCID 0000-0002-9777-6221

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Jon C.D. Houtman · 2000 to 2026
$70.0M
NCI NIH HHS P30 CA086862
6 · The paper itself

Abstract

Fibroblast growth factor receptor (FGFR) alterations drive oncogenesis in multiple tumor types. Here we studied pemigatinib, a selective, potent, oral FGFR1-FGFR3 inhibitor, in the phase 2 FIGHT-207 basket study of FGFR-altered advanced solid tumors. Primary end points were objective response rate (ORR) in cohorts A (fusions/rearrangements, n = 49) and B (activating non-kinase domain mutations, n = 32). Secondary end points were progression-free survival, duration of response and overall survival in cohorts A and B, and safety. Exploratory end points included ORR of cohort C (kinase domain mutations, potentially pathogenic variants of unknown significance, n = 26) and analysis of co-alterations associated with resistance and response. ORRs for cohorts A, B and C were 26.5% (13/49), 9.4% (3/32) and 3.8% (1/26), respectively. Tumors with no approved FGFR inhibitors or those with alterations not previously confirmed to be sensitive to FGFR inhibition had objective responses. In cohorts A and B, the median progression-free survival was 4.5 and 3.7 months, median duration of response was 7.8 and 6.9 months and median overall survival was 17.5 and 11.4 months, respectively. Safety was consistent with previous reports. The most common any-grade treatment-emergent adverse events were hyperphosphatemia (84%) and stomatitis (53%). TP53 co-mutations were associated with lack of response and BAP1 alterations with higher response rates. FGFR1-FGFR3 gatekeeper and molecular brake mutations led to acquired resistance. New therapeutic areas for FGFR inhibition and drug failure mechanisms were identified across tumor types. ClinicalTrials.gov identifier: NCT03822117 .

Indexed as

NeoplasmsPyrimidinesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3AdultAgedDrug Resistance, NeoplasmFemaleHumansMaleMiddle AgedMorpholinesMutationProgression-Free SurvivalProtein Kinase InhibitorsPyrrolesFGFR1 protein, humanFGFR3 protein, humanMorpholinespemigatinibProtein Kinase InhibitorsPyrimidinesPyrrolesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 3

Identifiers

PMID38710951
PMCPMC11186762

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.