Single Patient Treatment Study for the Use of XL999 Administered Intravenously to a Subject With Advanced Malignancies Previously Enrolled in Study XL999-900

Cancer is a worldwide clinical and economic problem. Conventional approaches to treating cancer include surgery, radiotherapy, and cytotoxic chemotherapy as single modalities or as combined therapies. Recently, targeted therapies including antibodies and small molecule inhibitors have also demonstrated clinical benefit. It is now possible to study different genetic lesions involved in cancer types due to advances in genomic methodologies. The investigational drug in this study, XL999 inhibits multiple receptor tyrosine kinases, including VEGF receptor (VEGFR2/KDR), platelet derived growth factor receptors (PDGFRβ), fms-like tyrosine kinase receptor 3 (FLT3), fibroblast growth factor receptors (FGFR1, FGFR3), RET, and KIT, and thus, interferes with multiple cellular processes simultaneously and will likely have effects on the integrity of tumor neovasculature and angiogenesis. Together with the ability to induce a novel cell cycle arrest, the spectrum of activities that XL999 exhibits may reduce both tumor cell proliferation and angiogenesis in the clinic.
The rationale and purpose of this maintenance study is to allow a subject receiving clinical benefit from XL999 to continue treatment.

开始日期2010-04-01

申办/合作机构

University of Texas Health Science Center At San Antonio

NCT00955084 / Completed临床1期

A Maintenance Study Evaluating the Long Term Safety of XL999 Administered Intravenously to Subjects With Advanced Malignancies Previously Enrolled in Other XL999 Studies

The primary objective of this study is to allow rollover of the two remaining subjects from the other XL999 studies to continue to receive XL999.
The secondary objectives of this study are as follows:
To evaluate tumor response after long term repeat administration of XL999 in two subjects rolled over from other XL999 studies.
To characterize the long term safety and tolerability of XL999 after repeat administration in two subjects rolled over from other XL999 studies.
To characterize the long term effects of XL999 on cardiac function after repeat administration in two subjects rolled over from other XL999 studies.

开始日期2008-08-01

申办/合作机构

Symphony Evolution, Inc.

NCT00491699 / Terminated临床1期

A Phase 1 Dose Escalation Study of the Safety, Pharmacokinetics, and Pharmacodynamics of XL999 Administered Intravenously to Subjects With Non-Small-Cell Lung Cancer (NSCLC)

The purpose of this study is to determine the safest dose of XL999 and how well subjects with Non-Small-Cell Lung Cancer tolerate XL999. XL999 is a small molecule inhibitor of multiple kinases including VEGFR, PDGFR, FGFR, FLT-3, and Src, which are involved in tumor cell growth, formation of new blood vessels (angiogenesis), and metastasis.

开始日期2007-08-01

申办/合作机构

Symphony Evolution, Inc.

100 项与 XL-999 相关的临床结果

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100 项与 XL-999 相关的转化医学

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100 项与 XL-999 相关的专利（医药）

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项与 XL-999 相关的文献（医药）

2011-07-15·Cancer Research1区 · 医学

VEGF and c-Met Blockade Amplify Angiogenesis Inhibition in Pancreatic Islet Cancer

1区 · 医学

Article

作者: Yao, Li-Chin ; Hashizume, Hiroya ; Williamson, Casey W. ; McDonald, Donald M. ; You, Weon-Kyoo ; Sennino, Barbara ; Falcón, Beverly ; Aftab, Dana T.

AbstractAngiogenesis inhibitors that block VEGF receptor (VEGFR) signaling slow the growth of many types of tumors, but eventually the disease progresses. Multiple strategies are being explored to improve efficacy by concurrent inhibition of other functionally relevant receptor tyrosine kinases (RTK). XL880 (foretinib, GSK1363089) and XL184 (cabozantinib) are small-molecule inhibitors that potently block multiple RTKs, including VEGFR and the receptor of hepatocyte growth factor c-Met, which can drive tumor invasion and metastasis. This study compared the cellular effects of XL880 and XL184 with those of an RTK inhibitor (XL999) that blocks VEGFR but not c-Met. Treatment of RIP-Tag2 mice with XL999 resulted in 43% reduction in vascularity of spontaneous pancreatic islet tumors over 7 days, but treatment with XL880 or XL184 eliminated approximately 80% of the tumor vasculature, reduced pericytes and empty basement membrane sleeves, caused widespread intratumoral hypoxia and tumor cell apoptosis, and slowed regrowth of the tumor vasculature after drug withdrawal. Importantly, XL880 and XL184 also decreased invasiveness of primary tumors and reduced metastasis. Overall, these findings indicate that inhibition of c-Met and functionally related kinases amplifies the effects of VEGFR blockade and leads to rapid, robust, and progressive regression of tumor vasculature, increased intratumoral hypoxia and apoptosis, and reduced tumor invasiveness and metastasis. Cancer Res; 71(14); 4758–68. ©2011 AACR.

2007-03-01·Methods and findings in experimental and clinical pharmacology

Gateways to clinical trials.

作者: Bayes, Miriam

Agomelatine, AGRO-100, AIDSVAX gp120 B/E, alfimeprase, aliskiren fumarate, ALVAC vCP1452, alvocidib hydrochloride, ambrisentan, AME-527, AN-0128, apadenoson, ARRY-142886, asenapine maleate, axitinib, azimilide hydrochloride; Belimumab, bevacizumab, biolimus A9, BiovaxID, bryostatin 1; Cannabidiol, celgosivir, CG-1940/CG-8711, CKD-501, collagen-PVP, CpG-10101, CTL-102, CTL-102/CB-1954; D-4F, darusentan, dexverapamil, DNA influenza vaccine, dronabinol/cannabidiol, dronedarone hydrochloride; Eculizumab, edodekin alfa, edotecarin, enzastaurin hydrochloride; Fingolimod hydrochloride; Golimumab; HBV-DNA vaccine, hyaluronic acid; I-131 ch-TNT-1/B, imatinib mesylate, inhaled insulin, ipilimumab, ispinesib mesylate, i.v. gamma-globulin; KU-59436; Lapaquistat; Mapatumumab, MC-1, MC-1/lisinopril, mepolizumab; Nibentan, nilotinib, Nobori, NV1FGF; Ocrelizumab; Paclimer, pagoclone, paliperidone, PC-515, PHA-794428, phosphostim, PPI-2458, prasugrel, PTC-299; Renzapride hydrochloride, Reolysin, reslizumab, revaprazan hydrochloride, rivaroxaban, romidepsin, rubitecan, ruboxistaurin mesilate hydrate; Sapacitabine, SarCNU, ST-1859, sunitinib malate; Tanespimycin, temsirolimus, tgAAC-94, TGN-255, ticagrelor, tipifarnib, tolvaptan, tretazicar, TRU-015; Upgrade varicella vaccine, Ushercell; Vernakalant hydrochloride, verpasep caltespen, VNP-40101M, VRC-HIVADV014-00-VP, VRC-HIVDNA009-00-VP, VX-001; XL-647, XL-820, XL-880, XL-999.

100 项与 XL-999 相关的药物交易

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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
急性髓性白血病	临床2期	美国	Symphony Evolution, Inc.	2006-05-01
复发性多发性骨髓瘤	临床2期	美国	Symphony Evolution, Inc.	2006-02-01
复发性卵巢癌	临床2期	美国	Symphony Evolution, Inc.	2006-01-01
转移性结直肠癌	临床2期	美国	Symphony Evolution, Inc.	2005-12-01
转移性肾细胞癌	临床2期	美国	Symphony Evolution, Inc.	2005-12-01
非小细胞肺癌	临床2期	美国	Symphony Evolution, Inc.	2005-12-01
晚期癌症	药物发现	美国	Symphony Evolution, Inc.	2008-08-01
肿瘤	药物发现	美国	Exelixis, Inc.	-

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


ASCO2007	临床2期	急性髓性白血病 \| 复发性卵巢癌 \| 多发性骨髓瘤 \| 非小细胞肺癌 \| 肾肿瘤 \| 转移性结直肠癌	79	XL999	(觸窪鏇憲糧網衊廠繭淵) = 壓鏇廠鏇獵製範夢艱糧淵鏇築醖廠膚膚餘糧襯 (選糧廠憲淵齋衊膚廠鹽 )	-	2007-06-20
ASCO2006	临床1期	晚期恶性实体瘤	15	XL999 2.4 mg/kg	(願觸範鹹築鬱醖簾構衊) = 願願膚願顧襯醖齋鬱鹽積鹽淵範夢膚獵網鏇鹽 (鏇艱壓鹽選製築鏇淵遞 ) 更多	-	2006-06-20