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Last update 05 Feb 2025
Cediranib
Last update 05 Feb 2025
Overview
Basic Info
Drug Type Small molecule drug |
Synonyms Cediranib (USAN/INN), Cediranib-maleate, Recentin + [4] |
Target |
Mechanism VEGFR1 antagonists(Vascular endothelial growth factor receptor 1 antagonists), VEGFR2 antagonists(Vascular endothelial growth factor receptor 2 antagonists), VEGFR3 antagonists(Vascular endothelial growth factor receptor 3 antagonists) |
Therapeutic Areas |
Inactive Indication |
Originator Organization |
Active Organization |
Inactive Organization |
Drug Highest PhasePhase 3 |
First Approval Date- |
RegulationOrphan Drug (US), Orphan Drug (EU) |
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Structure/Sequence
Molecular FormulaC25H27FN4O3 |
InChIKeyXXJWYDDUDKYVKI-UHFFFAOYSA-N |
CAS Registry288383-20-0 |
Related
111
Clinical Trials associated with CediranibNCT04739800
A Randomized Phase II Trial of Triplet Therapy (A PD-L1 Inhibitor Durvalumab (MEDI4736) in Combination With Olaparib and Cediranib) Compared to Olaparib and Cediranib or Durvalumab (MEDI4736) and Cediranib or Standard of Care Chemotherapy in Women With Platinum-Resistant Recurrent Epithelial Ovarian Cancer, Primary Peritoneal or Fallopian Cancer Who Have Received Prior Bevacizumab
NCT04090567
Overcoming PARP Inhibitor Resistance in BRCA Germline Mutation Positive Advanced Breast Cancer
NCT03741426
WIndow of Opportunity Clinical Trials Platform for Evaluation of Novel Treatments Strategies in REnal Cell Cancer
100 Clinical Results associated with Cediranib
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100 Translational Medicine associated with Cediranib
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100 Patents (Medical) associated with Cediranib
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701
Literatures (Medical) associated with Cediranib01 Jan 2025Cancer Genomics & Proteomics
Regulation and Function of CCL2 and N-Myc in Retinoic Acid-treated Neuroblastoma Cells
Article
Author: Bruckmueller, Henrike ; Kaehler, Meike ; Schmidt, Berit ; Issa, Reema Sami ; Murra, Nanke ; Waetzig, Vicki ; Pommert, Nina Sophie ; Tim, Vera ; Cascorbi, Ingolf
BACKGROUND/AIM:
Treatment with retinoic acid (RA) often promotes neuroblastoma differentiation and growth inhibition, including the suppression of the expression of the MYCN oncogene. However, RA also targets protumoral chemokines, such as CCL2, which may contribute to the development of resistance. The present study aimed to investigate the regulation and function of CCL2 and N-Myc in RA-treated neuroblastoma cells.
MATERIALS AND METHODS:
In Kelly or SH-SY5Y cells, viability was quantified by cell fitness assays. Expression was analyzed using quantitative PCR and the regulation of proteins using enzyme-linked immunoabsorbent assays (ELISA) or western blots.
RESULTS:
In MYCN-amplified Kelly cells, endogenous CCL2 levels were significantly lower compared to MYCN non-amplified SH-SY5Y cells. Treatment with 5 μM RA increased CCL2 release in both cell lines, but reduced N-Myc levels and cell numbers in Kelly cells. Over-expression of MYCN enhanced viability in SH-SY5Y cells, but did not affect RA-induced CCL2 release, while supplementation of CCL2 in Kelly cells did not prevent RA-mediated growth reduction. Impaired N-Myc or CCL2 signaling reduced the survival of all RA-treated cells and inhibition of N-Myc also decreased CCL2 levels. However, attenuated survival signaling was not generally associated with reduced levels of N-Myc or CCL2. Co-application of RA and the growth factor receptor inhibitors cediranib or crizotinib decreased N-Myc levels only in Kelly cells, while CCL2 release was dependent on the cell type and stimulus.
CONCLUSION:
CCL2 and N-Myc promote the viability of RA-treated cells, although the levels of these mediators were not consistently correlated with cellular outcomes, especially during apoptotic signaling.
20 Dec 2024JOURNAL OF CLINICAL ONCOLOGY
Cediranib and Olaparib Combination Compared With Cediranib or Olaparib Alone, or Chemotherapy in Platinum-Resistant or Primary Platinum-Refractory Ovarian Cancer: NRG-GY005
Article
Author: Kohn, Elise C. ; Brady, Mark F. ; McDonald, Megan E. ; Duska, Linda R. ; Kavecansky, Juraj ; Moore, Richard G. ; Lheureux, Stephanie ; Rose, Peter G. ; McNally, Leah ; Provencher, Michèle ; MacKay, Helen ; Street, Daron ; Miller, Austin ; Wenzel, Lari B. ; Cantuaria, Guilherme ; Kim, Yong-Man ; Bookman, Michael A. ; Lee, Jung-Min ; Powell, Matthew ; Lea, Jayanthi ; Secord, Angeles Alvarez ; Huang, Helen Q. ; Leath, Charles A. ; Cadungog, Mark G.
PURPOSE:
We assessed the efficacy of cediranib, olaparib, and cediranib/olaparib compared with standard-of-care chemotherapy (SOC) in platinum-resistant or platinum-refractory epithelial ovarian cancer (PROC).
PATIENTS AND METHODS:
NRG-GY005 is an open-label, four-arm, phase II/III superiority trial enrolling patients with high-grade serous/endometrioid PROC and one to three previous therapies. Key exclusion criteria included previous receipt of poly(ADP-ribose) polymerase inhibitor or receipt of antiangiogenic therapy in the recurrent setting. Treatment arms (SOC [once weekly paclitaxel, topotecan, or pegylated liposomal doxorubicin], cediranib, olaparib, or cediranib/olaparib) were equally randomized. A preplanned interim futility analysis on the basis of progression-free survival (PFS) selected treatment arms to advance to phase III. PFS and overall survival (OS) were phase III coprimary end points, with hierarchical testing of PFS followed by OS to preserve type 1 error control, designed to have 90% power for a 0.625 PFS hazard ratio (HR). OS was tested after PFS in the multiple hierarchical testing procedure. Secondary end points included objective response rate (ORR) and patient-reported outcomes.
RESULTS:
Five hundred sixty-two eligible patients were enrolled for phase II/III. Three arms met PFS criteria to carry forward to phase III (SOC, cediranib/olaparib, and cediranib). Median PFS was 3.4, 5.2, and 4 months with SOC, cediranib/olaparib, and cediranib, respectively, with a median follow-up duration of 42.2 months. PFS HR estimates for cediranib/olaparib and cediranib (
v
SOC) were 0.796 (98.3% CI, 0.597 to 1.060) and 0.972 (98.3% CI, 0.726 to 1.300), respectively. Median OS was 13.6, 12.8, and 10.5 months, and of 443 patients with measurable disease, ORR was 8.6%, 24.7%, and 13.1% for SOC, cediranib/olaparib, and cediranib, respectively. No new safety signals were identified. In patients receiving cediranib/olaparib, no statistically significant difference was observed on the NFOSI-DRS-P subscale compared with SOC (98.3% CI, –1.3 to 1.5,
P
= .8725).
CONCLUSION:
The cediranib-containing arms demonstrated clinical activity on the basis of PFS but were not superior compared with SOC.
01 Nov 2024Clinical Lung Cancer
A Phase I Open-Label Study of Cediranib Plus Etoposide and Cisplatin as First-Line Therapy for Patients With Extensive-Stage Small-Cell Lung Cancer or Metastatic Neuroendocrine Non–Small-Cell Lung Cancer
Article
Author: Camidge, D Ross ; Concannon, Kyle F ; Marotti, Marcelo ; Concannon, Kyle F. ; Glisson, Bonnie S. ; Camidge, D. Ross ; Doebele, Robert C. ; Camidge, D.Ross ; Heymach, John V. ; Doebele, Robert C ; Glisson, Bonnie S ; Heymach, John V ; Huang, Chao
INTRODUCTION:
Small cell lung cancer (SCLC) is known to express high levels of the proangiogenic factor vascular endothelial growth factor (VEGF). We assessed the safety and tolerability of cediranib, an oral inhibitor of VEGF receptor tyrosine kinases, in combination with etoposide and cisplatin as first-line therapy for extensive-stage (ES) SCLC or metastatic lung neuroendocrine cancer (NEC).
METHODS:
Patients received up to six 21-day cycles of etoposide (100 mg/m2, days 1-3) and cisplatin (80 mg/m2, day 1) with once-daily cediranib until disease progression or unacceptable toxicity. Cediranib dosing started at 30 mg with de-escalation cohorts planned based on cycle 1 dose-limiting toxicities (DLTs). An expansion cohort of 12 patients was enrolled at the recommended phase II dose.
RESULTS:
Twenty-two patients (18 with ES SCLC, 4 with NEC) received treatment. Only 4 patients were enrolled at the 30 mg cediranib dose before other studies established 20 mg/day as the recommended dose with chemotherapy. Among the 18 patients enrolled at the 20-mg dose, common adverse events included nausea/vomiting, neutropenia, and diarrhea; 8 patients (44%) had grade 1 or 2 hypertension, and 2 (11%) had grade 3 hemoptysis. For all 18 patients, the objective response rate and median progression-free survival duration were 67% and 7.9 months. Plasma levels of VEGF were significantly higher, and those of soluble VEGFR2 were significantly lower, on day 22 than at baseline but were not correlated with tumor shrinkage.
CONCLUSIONS:
Cediranib (20 mg) plus etoposide and cisplatin is well tolerated and has promising clinical activity.
100 Deals associated with Cediranib
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R&D Status
10 top R&D records. to view more data
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| Indication | Highest Phase | Country/Location | Organization | Date |
|---|---|---|---|---|
| Ovarian Cancer | NDA/BLA | - | - | |
| Ovarian Serous Adenocarcinoma | Phase 3 | US | 03 May 2016 | |
| Ovarian Serous Adenocarcinoma | Phase 3 | JP | 03 May 2016 | |
| Ovarian Serous Adenocarcinoma | Phase 3 | CA | 03 May 2016 | |
| Ovarian Serous Adenocarcinoma | Phase 3 | PR | 03 May 2016 | |
| Ovarian Serous Adenocarcinoma | Phase 3 | KR | 03 May 2016 | |
| Platinum-Resistant Primary Peritoneal Carcinoma | Phase 3 | US | 03 May 2016 | |
| Platinum-Resistant Primary Peritoneal Carcinoma | Phase 3 | JP | 03 May 2016 | |
| Platinum-Resistant Primary Peritoneal Carcinoma | Phase 3 | CA | 03 May 2016 | |
| Platinum-Resistant Primary Peritoneal Carcinoma | Phase 3 | PR | 03 May 2016 |
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Clinical Result
Clinical Result
Indication
Phase
Evaluation
View All Results
Phase 2 | 123 | (Arm A) | lmaxhcmmpb(zkcgfdfqpv) = scyacigiby kulyiayfcw (sygerpbyrm, vqkpppejhb - btlrkveytq) View more | - | 10 Jan 2025 | ||
lmaxhcmmpb(zkcgfdfqpv) = fedxeznkbb kulyiayfcw (sygerpbyrm, vnbozykooq - zhtbiveiwi) View more | |||||||
Phase 2/3 | Platinum-Resistant Ovarian Carcinoma high-grade serous | endometrioid | - | rmlzhfpxdo(hnqeotqejf) = bkzjwkewvq jywxivgyjk (tfvgktpbnc ) View more | Negative | 20 Dec 2024 | ||
rmlzhfpxdo(hnqeotqejf) = ratsmqumfl jywxivgyjk (tfvgktpbnc ) View more | |||||||
Phase 2 | 34 | AZD2171 (Cediranib) (AZD2171 (Cediranib) 30 mg) | apgbbfrnds(ukutqvwybt) = gobanzbzkc cxubhjwkfr (xzmuvioqnr, fxvtqfjlov - xcjwrbdlid) View more | - | 19 Sep 2024 | ||
AZD2171 (Cediranib)+Sunitinib Malate (AZD2171 (Cediranib) 30 mg Followed by Sunitinib Malate 37.5 mg) | apgbbfrnds(ukutqvwybt) = ztysbwihle cxubhjwkfr (xzmuvioqnr, cshngjruui - mmolnuajlv) View more | ||||||
Phase 2 | 124 | nmwmszlnbb(toikbzkarr) = aodgmfrvfi odenmzhyop (qpgwzlhyzw ) View more | - | 10 Mar 2024 | |||
nmwmszlnbb(toikbzkarr) = svyvsjpken odenmzhyop (qpgwzlhyzw ) View more | |||||||
Phase 2 | 70 | fopixffsqk(cbtxyolddh) = gwupdapblz okphyfjype (lblgvobrvw, mheplliint - byajjskopt) View more | - | 02 Feb 2024 | |||
(Arm B (Bevacizumab)) | fopixffsqk(cbtxyolddh) = edefoxxzrp okphyfjype (lblgvobrvw, ycantimegq - uwyrnpffhg) View more | ||||||
Phase 3 | 565 | (Standard of care (SOC)) | wvcmlxzcel(whwwyfpxub) = ksnjrtukoh bqvyejwack (sglxdvskwv ) | Negative | 22 Oct 2023 | ||
Olaparib (O) | wvcmlxzcel(whwwyfpxub) = uwsluvyqpa bqvyejwack (sglxdvskwv ) | ||||||
Phase 2 | 97 | overall | ixfmfbadsv(lavppgfdzi) = mgafwsqgig fgxuqsypcf (ydhybgzzmf ) | Negative | 31 May 2023 | ||
ixfmfbadsv(lavppgfdzi) = gtrropmkqa fgxuqsypcf (ydhybgzzmf ) View more | |||||||
Phase 2 | Metastatic endometrial cancer Maintenance | - | rigbnfgfdv(duutvmpfzc) = iajgiwfpsp tjpwxsdbvm (wqjrupqxxt ) | - | 31 May 2023 | ||
Phase 2 | - | hocxjqugim(exlkjthwtg) = yuqgmwihda yzofdlshvo (msotkjumpu, 10.7 - NR) View more | - | 31 May 2023 | |||
Phase 2 | 70 | Cediranib/Olaparib | rjrtwkykcf(scmceypzuk) = vgfjhqhzvb jdmbpxtgqd (icscjswqus ) View more | Negative | 14 Nov 2022 | ||
Bevacizumab | rjrtwkykcf(scmceypzuk) = mckzmtkivl jdmbpxtgqd (icscjswqus ) View more |
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