Delving into the Latest Updates on Cediranib with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Cediranib (USAN/INN), Cediranib-maleate, Recentin

+ [4]

Target

VEGFR1 x VEGFR2 x VEGFR3

Action

antagonists

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

NeoplasmsNervous System DiseasesDigestive System Disorders+ [5]

Active Indication

Endometrioid carcinoma ovaryFallopian Tube Clear Cell AdenocarcinomaOvarian clear cell adenocarcinoma+ [61]

Inactive Indication

acute leukemiaAcute Lymphoblastic LeukemiaAcute myeloid leukaemia with 11q23 abnormality+ [118]

Originator Organization

AstraZeneca PLC

Active Organization

National Cancer Institute

AstraZeneca PLC

Inactive Organization

University College LondonWyeth AB

AstraZeneca Pharmaceuticals Co. Ltd.

Drug Highest PhasePhase 3

First Approval Date-

RegulationOrphan Drug (European Union)

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Structure/Sequence

Molecular FormulaC25H27FN4O3

InChIKeyXXJWYDDUDKYVKI-UHFFFAOYSA-N

CAS Registry288383-20-0

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

This phase II trial studies the possible benefits of treatment with different combinations of the drugs durvalumab, olaparib and cediranib vs. the usual treatment in patients with ovarian, primary peritoneal, or fallopian tube cancer that has come back after a period of improvement with platinum therapy (recurrent platinum resistant). Usual treatment is the type of treatment most patients with this condition receive if they are not part of a clinical study. Combination therapies studied in this trial include MEDI4736 (durvalumab) plus olaparib and cediranib, durvalumab and cediranib, or olaparib and cediranib. Monoclonal antibodies, such as durvalumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumors cells to grow and spread. Olaparib is an inhibitor of PARP, an enzyme that helps repair deoxyribonucleic acid (DNA) when it becomes damaged. Blocking PARP may help keep cancer cells from repairing their damaged DNA, causing them to die. PARP inhibitors are a type of targeted therapy. Cediranib may stop the growth of tumor cells by blocking VEGF (an enzyme). needed for cell growth. Giving different combinations of durvalumab, olaparib and cediranib may work better in increasing the duration of time that the cancer does not progress compared to the usual treatment.

Start Date10 Jun 2021

Sponsor / Collaborator

National Cancer Institute

[+1]

NCT04090567

/ RecruitingPhase 2IIT

Overcoming PARP Inhibitor Resistance in BRCA Germline Mutation Positive Advanced Breast Cancer

This phase II trial studies how well olaparib with cediranib or AZD6738 works in treating patients with germline BRCA mutated breast cancer that has spread to other places in the body (advanced or metastatic). Olaparib, cediranib, and AZD6738 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

Start Date28 Jul 2020

Sponsor / Collaborator

The University of Texas MD Anderson Cancer Center

[+1]

NCT03741426

/ RecruitingPhase 2IIT

WIndow of Opportunity Clinical Trials Platform for Evaluation of Novel Treatments Strategies in REnal Cell Cancer

Evaluation of proof of mechanism with relation to ktrans and/or CD8 count when 3 different IMPs are given as monotherapy or as combination therapy. These would be administered in the "window of opportunity", prior to nephrectomy in surgically resectable renal cell cancer

Start Date27 Jul 2020

Sponsor / Collaborator

Cambridge University Hospitals NHS Foundation Trust

[+3]

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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711

Literatures (Medical) associated with Cediranib

01 Jan 2025·Cancer Genomics - Proteomics

Regulation and Function of CCL2 and N-Myc in Retinoic Acid-treated Neuroblastoma Cells

Article

Author: Bruckmueller, Henrike ; Schmidt, Berit ; Tim, Vera ; Pommert, Nina Sophie ; Murra, Nanke ; Kaehler, Meike ; Issa, Reema Sami ; Cascorbi, Ingolf ; Waetzig, Vicki

BACKGROUND/AIMTreatment 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 METHODSIn 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.RESULTSIn 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.CONCLUSIONCCL2 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 2024·Journal 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: Provencher, Michèle ; McDonald, Megan E. ; Kavecansky, Juraj ; Kohn, Elise C. ; Lheureux, Stephanie ; Duska, Linda R. ; Huang, Helen Q. ; Cantuaria, Guilherme ; Kim, Yong-Man ; MacKay, Helen ; Moore, Richard G. ; Lea, Jayanthi ; Rose, Peter G. ; Leath, Charles A. ; McNally, Leah ; Brady, Mark F. ; Cadungog, Mark G. ; Street, Daron ; Miller, Austin ; Secord, Angeles Alvarez ; Powell, Matthew ; Wenzel, Lari B. ; Lee, Jung-Min ; Bookman, Michael A.

PURPOSEWe 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 METHODSNRG-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). CONCLUSIONThe cediranib-containing arms demonstrated clinical activity on the basis of PFS but were not superior compared with SOC.

01 Dec 2024·Science Bulletin

Restoring sweat gland function in mice using regenerative sweat gland cells derived from chemically reprogrammed human epidermal keratinocytes

Article

Author: Wu, Lu ; Chen, Huating ; Xiang, Jiangbing ; Zhang, Hongliang ; Fu, Xiaobing ; Cui, Shaoyuan ; Li, Yan ; Dong, Lei ; Ji, Shuaifei ; Pi, Wei ; Sun, Xiaoyan

The regeneration of sweat glands (SwGs) plays a pivotal role in the functional recovery of extensive skin wounds. Recent research has illuminated the possibility of reprogramming human epidermal keratinocytes (HEKs) into induced SwG cells through the ectopic expression of ectodysplasin A. However, the clinical application of this genetic manipulation approach is inherently limited. In this study, we present findings demonstrating that a combination of six compounds can effectively and speedily reprogram HEKs in culture into fully functional SwG cells. These chemically induced SwG-like cells (ciSGCs) closely resemble the morphology, phenotypes, and functional properties of human primary SwG ductal cells. Furthermore, ciSGCs can be stimulated to differentiate into mature SwG cell types in vitro. In a 3D culture system, they can also generate SwG organoids that exhibit structural and biological features akin to native SwGs. Upon transplantation into scalded mouse paw skin, ciSGCs significantly expedited cutaneous wound healing and completely restored the structural and functional aspects of the SwGs. In conclusion, the small molecule cocktail-directed SwG reprogramming offers a non-transgenic and controllable strategy for producing high-quality, clinical-grade SwG cells, showing immense potential for the treatment of burn patients.

100 Deals associated with Cediranib

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External Link

KEGG	Wiki	ATC	Drug Bank
D08881	Cediranib	L01XE32	DB04849

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Metastatic Colorectal Carcinoma	Phase 2	United States	AstraZeneca PLC	30 Aug 2006
Metastatic Colorectal Carcinoma	Phase 2	Israel	AstraZeneca PLC	30 Aug 2006
Glioblastoma	Phase 2	European Union	AstraZeneca PLC	-
Glioblastoma	Phase 2	Canada	AstraZeneca PLC	-
Ovarian Cancer	Phase 2	-	AstraZeneca Pharmaceuticals Co. Ltd.	-
Metastatic Colorectal Carcinoma	Discovery	Israel	AstraZeneca PLC	30 Aug 2006
Metastatic Colorectal Carcinoma	Discovery	United States	AstraZeneca PLC	30 Aug 2006
Glioblastoma	Discovery	Canada	AstraZeneca PLC	-
Glioblastoma	Discovery	European Union	AstraZeneca PLC	-
Ovarian Cancer	Discovery	-	AstraZeneca Pharmaceuticals Co. Ltd.	-

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03314740 (IRFMN-OVA-7289, EudraCT: 2016-003964-38 \| IRFMN-OVA-7289 \| BAROCCO, CTgov)	Phase 2	Recurrent ovarian cancer \| Platinum-Resistant Primary Peritoneal Carcinoma	123	Paclitaxel (Arm A)	humprxlinr(nkrvgdncdc) = fsqkjprqzr asjqxyytyc (nushusceqd, unasfxlvpt - fbqmriryyp) View more	-	10 Jan 2025
				Olaparib+Cediranib (Arm B)	humprxlinr(nkrvgdncdc) = otukqwryza asjqxyytyc (nushusceqd, ovizwcmkjz - bxmjtfdoaq) View more
NCT02502266 (NRG-GY005, Pubmed \| J Clin Oncol)	Phase 2/3	Platinum-Resistant Ovarian Carcinoma high-grade serous \| endometrioid	-	Cediranib	(okowiajcxf) = rdfsstuzlm tqysweuuad (cxbvafcfia ) View more	Negative	20 Dec 2024
				Olaparib	(okowiajcxf) = kvipumwlsw tqysweuuad (cxbvafcfia ) View more
EUCTR2017-000161-75 (ICON9, ESMO2024) Manual	Phase 3	Platinum-Sensitive Ovarian Carcinoma Maintenance	337	Olaparib 300mg twice daily + Cediranib 20mg once daily	(mbzceseanz) = oscbbffred lhvjnfbyjr (rzjtiruliv, 11.3 - 16.1) View more	Negative	16 Sep 2024
				Olaparib 300mg twice daily	(mbzceseanz) = swcneelkax lhvjnfbyjr (rzjtiruliv, 8.4 - 12.8) View more
407 (ESGO2024)	Phase 2	Recurrent Endometrial Cancer	124	Weekly paclitaxel	(exekhxfrbu) = ypoqqxkslk psxpxruynh (joqsnigwmj ) View more	-	10 Mar 2024
				Weekly paclitaxel + Cediranib	(exekhxfrbu) = bhrdeioxya psxpxruynh (joqsnigwmj ) View more
NCT02974621 (CTgov)	Phase 2	Recurrent Glioblastoma	70	Olaparib+Cediranib (Arm A (Olaparib, Cediranib Maleate))	fypdizrjya(jbucbzyiyl) = sdqpchvwtp afmkjosnfk (uewjrbpdae, ovtzveweoz - qqnsxpiptx) View more	-	02 Feb 2024
				Bevacizumab (Arm B (Bevacizumab))	fypdizrjya(jbucbzyiyl) = glmrqoowwb afmkjosnfk (uewjrbpdae, buqmcwetdy - rxlvnncjpv) View more
NCT04739800 (NRG-GY023, ESMO 12023 \| ESMO 22023) Manual	Phase 2	Platinum-Resistant Ovarian Carcinoma	103	Durvalumab+Olaparib+Cediranib (DOC)	(ftgtuqhdzd) = wlxpwlaaih zskrupwymz (miqoaeeqhu, 2 - 4.2)	Negative	22 Oct 2023
				Olaparib+Cediranib (OC)	(ftgtuqhdzd) = lkwmzipiqf zskrupwymz (miqoaeeqhu, 2.1 - 3.9)
NCT02446600 (NRG-GY004, ESMO2023)	Phase 3	Platinum-Sensitive Primary Peritoneal Carcinoma \| Ovarian Serous Tumor \| Fallopian Tube Clear Cell Adenocarcinoma \| Ovarian mixed epithelial carcinoma \| Recurrent ovarian cancer \| Recurrent Primary Peritoneal Carcinoma \| Undifferentiated Ovarian Carcinoma \| Endometrioid carcinoma ovary \| Ovarian clear cell adenocarcinoma \| Transitional Cell Carcinoma gBRCAm	565	cediranib (Standard of care (SOC))	(smixwzxuqt) = wkwyoxavsl vvjylsphji (wfhdftevuw )	Negative	22 Oct 2023
				Olaparib (O)	(smixwzxuqt) = kyohoewjtc vvjylsphji (wfhdftevuw )
NCT03851614 (ASCO_Breakthrough2023) Manual	Phase 2	Advanced Colorectal Adenocarcinoma \| Advanced Pancreatic Adenocarcinoma pMMR	31	durvalumab+olaparib (pMMR-CRC)	yaeftwpkif(mlxumqxrzq) = Increased CD8+ tumor-infiltrating lymphocytes (TILs) at baseline (p=0.04) and at C2 (p=0.023) and low baseline CD68+ cells (p=0.018) were associated with longer OS. nwwvemnzcn (wgdtcwnqjj )	Negative	03 Aug 2023
				durvalumab+cediranib (pMMR-CRC)
NCT03660826 (NRG GY012, ASCO2023) Manual	Phase 2	Advanced Endometrial Carcinoma	97	overall	fujetagkds(siybzwpyzd) = eyzyyrisnh ihyudkwscl (aglbbfagzf )	Negative	31 May 2023
				Cediranib or Cediranib + Olaparib (IL-6 > 4 pg/ml)	fujetagkds(siybzwpyzd) = etbwfjsboo ihyudkwscl (aglbbfagzf ) View more
NCT03851614 (DAPPER, ASCO2023)	Phase 2	Leiomyosarcoma	-	Durvalumab plus Cediranib	(ybeufufjhi) = qwatumdrbb skegesczkd (dgdzjxtujs, 10.7 - NR) View more	-	31 May 2023