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NCT02791919
Wee1 Kinase Inhibitor AZD1775 and Combination Chemotherapy in Treating Children, Adolescents and Young Adults With Relapsed or Refractory Acute Myeloid Leukemia
Phase 1 trial testing Cytarabine in CNS 2a. Withdrawn.
31 May 2019
Quick facts
| Lead sponsor | National Cancer Institute (NCI) |
|---|---|
| Phase | Phase 1 |
| Status | Withdrawn |
| Study type | INTERVENTIONAL |
| Allocation | na |
| Design | single group |
| Masking | none |
| Primary purpose | treatment |
| Start date | 25 May 2017 |
| Primary completion | 31 May 2019 |
| Estimated completion | 31 May 2019 |
Drugs / interventions tested
- Cytarabine — full drug profile →
- Filgrastim
- Fludarabine Phosphate (FLUDARABINE PHOSPHATE) — full drug profile →
- Laboratory Biomarker Analysis
- Pharmacological Study — full drug profile →
- WEE1 Inhibitor AZD1775
Conditions studied
- CNS 2a — all drugs for CNS 2a →
- CNS 2b — all drugs for CNS 2b →
- CNS 2c — all drugs for CNS 2c →
- CNS1 — all drugs for CNS1 →
Sponsor
National Cancer Institute (NCI)
Who can join
Adults 1 to 21, any sex, with CNS 2a or CNS 2b. Patients with the condition only — healthy volunteers not accepted.
Sponsor's own description
This phase I trial studies the side effects and best dose of wee1 kinase inhibitor AZD1775 when given together with fludarabine, cytarabine, and filgrastim (FLAG) combination chemotherapy in treating children, adolescents and young adults with relapsed or refractory acute myeloid leukemia. Wee1 kinase inhibitor AZD1775 may help combination chemotherapy work better by making tumor cells more sensitive to the drugs. Drugs used in chemotherapy, such as fludarabine and cytarabine, may prevent tumor cells from multiplying by damaging their deoxyribonucleic acid (DNA), which in turn stops the tumor from growing. Giving wee1 kinase inhibitor AZD1775 and FLAG chemotherapy may work better in treating patients with acute myeloid leukemia.
Publications & conference data
5 peer-reviewed publications reference this trial (live from Europe PMC):
-
A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target.
Ghelli Luserna di Rorà A, Cerchione C, Martinelli G, Simonetti G. · · 2020 · cited 232× · PMID 32958072 · DOI 10.1186/s13045-020-00959-2 -
Synthetic and Medicinal Chemistry Approaches Toward WEE1 Kinase Inhibitors and Its Degraders.
Alli VJ, Yadav P, Suresh V, Jadav SS. · · 2023 · cited 18× · PMID 37323408 · DOI 10.1021/acsomega.3c01558 -
Advancing cancer therapy: new frontiers in targeting DNA damage response.
Qian J, Liao G, Chen M, Peng RW, et al · · 2024 · cited 16× · PMID 39372203 · DOI 10.3389/fphar.2024.1474337 -
Targeting the DNA damage response in cancer.
Federica G, Michela C, Giovanna D. · · 2024 · cited 12× · PMID 39492835 · DOI 10.1002/mco2.788 -
The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.
Rouault CD, Charafe-Jauffret E, Ginestier C. · · 2025 · cited 3× · PMID 41028732 · DOI 10.1038/s41467-025-64445-4
Verify or expand the search:
- PubMed search for NCT02791919
- Europe PMC full search
- ASCO Meeting Library
- ESMO Meeting Library
- bioRxiv preprints
- medRxiv preprints
- Google Scholar
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Verify against primary sources
- ClinicalTrials.gov — authoritative US registry record
- WHO ICTRP — international registry index
- EU Clinical Trials Register
- Sponsor press releases (Google)
- Trial protocol + status: ClinicalTrials.gov NCT02791919 (US National Library of Medicine, public domain)
- Publications: Europe PMC API search by NCT ID, retrieved 10 June 2026
- Drug + disease cross-links: matched in real time against Drug Landscape's normalised drug + company + condition tables
- Sponsor: as reported to ClinicalTrials.gov by National Cancer Institute (NCI)
- Last refreshed: 3 May 2017
Drug Landscape aggregates and links these public records for informational use only. Always verify against the primary source before clinical or regulatory decisions. Canonical URL: https://druglandscape.com/trial/NCT02791919.
Primary sources · FDA · ClinicalTrials.gov · EMA · SEC EDGAR · ChEMBL · Wikidata · full sourcing