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Journal of Clinical Oncology | 2008

Phase II Study of Sunitinib Malate, an Oral Multitargeted Tyrosine Kinase Inhibitor, in Patients With Metastatic Breast Cancer Previously Treated With an Anthracycline and a Taxane

Harold J. Burstein; Anthony D. Elias; Hope S. Rugo; Melody A. Cobleigh; Antonio C. Wolff; Peter D. Eisenberg; Mary Lehman; Bonne J. Adams; Carlo L. Bello; Samuel E. DePrimo; Charles M. Baum; Kathy D. Miller

PURPOSE Sunitinib is an oral, multitargeted tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, stem cell factor receptor (KIT), and colony-stimulating factor-1 receptor. This phase II, open-label, multicenter study evaluated sunitinib monotherapy in patients with metastatic breast cancer (MBC). PATIENTS AND METHODS Sixty-four patients previously treated with an anthracycline and a taxane received sunitinib 50 mg/d in 6-week cycles (4 weeks on, then 2 weeks off treatment). The primary end point was objective response rate. Plasma samples were obtained for pharmacokinetic and biomarker analysis. RESULTS Seven patients achieved a partial response (median duration, 19 weeks), giving an overall response rate of 11%. Three additional patients (5%) maintained stable disease for >or= 6 months. Median time to progression and overall survival were 10 and 38 weeks, respectively. Notably, responses occurred in triple negative tumors and HER2-positive, trastuzumab-treated patients. Thirty-three patients (52%) required dose interruption during >or= 1 cycle, and 25 patients required dose reduction (39%). Thirty-six patients (56%) had dose modifications due to adverse events (AEs). Treatment was associated with increases in plasma VEGF and decreases in soluble VEGFRs and KIT. The most common AEs were fatigue, nausea, diarrhea, mucosal inflammation, and anorexia. Most AEs were mild to moderate (grade 1 to 2) in severity and were effectively managed with dose delays or reductions. CONCLUSION Sunitinib is active in patients with heavily pretreated MBC. Most AEs were of mild-to-moderate severity and manageable with supportive treatment and/or dose modification. Further studies in breast cancer are warranted.


Clinical Cancer Research | 2012

A Phase I First-in-Human Study of TRC105 (Anti-Endoglin Antibody) in Patients with Advanced Cancer

Lee S. Rosen; Herbert Hurwitz; Michael K. Wong; Jonathan W. Goldman; David S. Mendelson; William D. Figg; Shawn D. Spencer; Bonne J. Adams; Delia Alvarez; Ben K. Seon; Charles P. Theuer; Bryan R. Leigh; Michael S. Gordon

Purpose: TRC105 is a chimeric IgG1 monoclonal antibody that binds CD105 (endoglin). This first-in-human, phase I, open-label study assessed safety, pharmacokinetics, and antitumor activity of TRC105 in patients with advanced refractory solid tumors. Patients and Methods: Patients received escalating doses of intravenous TRC105 until disease progression or unacceptable toxicity using a standard 3 + 3 phase I design. Results: Fifty patients were treated with escalating doses of TRC105. The maximum tolerated dose (MTD) was exceeded at 15 mg/kg every week because of dose-limiting hypoproliferative anemia. TRC105 exposure increased with increasing dose, and continuous serum concentrations that saturate CD105 receptors were maintained at 10 mg/kg weekly (the MTD) and 15 mg/kg every 2 weeks. Common adverse events including anemia, telangiectasias, and infusion reactions reflected the mechanism of action of the drug. Antibodies to TRC105 were not detected in patients treated with TRC105 from Chinese hamster ovary cells being used in ongoing phase Ib and phase II studies. Stable disease or better was achieved in 21 of 45 evaluable patients (47%), including two ongoing responses at 48 and 18 months. Conclusion: TRC105 was tolerated at 10 mg/kg every week and 15 mg/kg every 2 weeks, with a safety profile that was distinct from that of VEGF inhibitors. Evidence of clinical activity was seen in a refractory patient population. Ongoing clinical trials are testing TRC105 in combination with chemotherapy and VEGF inhibitors and as a single agent in prostate, ovarian, bladder, breast, and hepatocellular cancer. Clin Cancer Res; 18(17); 4820–9. ©2012 AACR.


Clinical Cancer Research | 2014

An Open-Label Phase Ib Dose-Escalation Study of TRC105 (Anti-Endoglin Antibody) with Bevacizumab in Patients with Advanced Cancer

Michael S. Gordon; Francisco Robert; Daniela Matei; David S. Mendelson; Jonathan W. Goldman; E. Gabriela Chiorean; Robert M. Strother; Ben K. Seon; William D. Figg; Cody J. Peer; Delia Alvarez; Bonne J. Adams; Charles P. Theuer; Lee S. Rosen

Purpose: Endoglin, an endothelial cell membrane receptor expressed on angiogenic tumor vessels, is essential for angiogenesis and upregulated in the setting of VEGF inhibition. TRC105 is an anti-endoglin IgG1 monoclonal antibody that potentiates VEGF inhibitors in preclinical models. This study assessed safety, pharmacokinetics, and antitumor activity of TRC105 in combination with bevacizumab. Experimental Design: Patients (n = 38) with advanced solid tumors, Eastern Cooperative Group performance status 0–1, and normal organ function were treated with escalating doses of TRC105 plus bevacizumab until disease progression or unacceptable toxicity using a standard 3 + 3 phase I design. Results: TRC105 and bevacizumab were well tolerated at their recommended single-agent doses (10 mg/kg) when the initial dose of TRC105 was delayed by one week and divided over 2 days to limit the frequency of headache. The concurrent administration of bevacizumab and TRC105 did not otherwise potentiate known toxicities of TRC105 or bevacizumab. Hypertension and proteinuria were observed, though not at rates expected for single-agent bevacizumab. Several patients who had previously progressed on bevacizumab or VEGF receptor tyrosine kinase inhibitor (VEGFR TKI) treatment experienced reductions in tumor volume, including two partial responses by RECIST, and 6 remained without progression for longer periods than during their prior VEGF inhibitor therapy. Conclusions: TRC105 was well tolerated with bevacizumab and clinical activity was observed in a VEGF inhibitor–refractory population. Ongoing clinical trials are testing TRC105 in combination with bevacizumab in glioblastoma and with VEGFR TKIs in renal cell carcinoma, hepatocellular carcinoma, and soft tissue sarcoma. Clin Cancer Res; 20(23); 5918–26. ©2014 AACR.


Cancer Medicine | 2014

Modulation of circulating protein biomarkers following TRC105 (anti-endoglin antibody) treatment in patients with advanced cancer

Yingmiao Liu; Mark D. Starr; John C. Brady; Andrew Dellinger; Herbert Pang; Bonne J. Adams; Charles P. Theuer; Nam Y. Lee; Herbert Hurwitz; Andrew B. Nixon

TRC105 is an endoglin‐targeting drug that possesses anti‐angiogenic and antitumor potential. Analysis of the initial phase I trial of TRC105 demonstrated good tolerability and efficacy in cancer patients. In this report, we analyzed multiple circulating biomarkers at baseline, cycle 2 day 1 (C2D1), and end of study (EOS) for each patient. The baseline level and the fold change from baseline to both C2D1 and EOS for each marker were statistically analyzed. At C2D1, seven markers were significantly downregulated (angiopoietin‐2 [Ang‐2], insulin‐like growth factor‐binding protein‐3 [IGFBP‐3], plasminogen activator inhibitor‐1 [PAI‐1] total, platelet‐derived growth factor [PDGF]‐AA, PDGF‐BB, thrombospondin‐1 [TSP‐1], and vascular endothelial growth factor [VEGF]‐D). Meanwhile, seven markers were upregulated by C2D1 (E‐Cadherin, soluble Endoglin [sEnd], E‐Selectin, interleukin‐6 [IL‐6], osteopontin [OPN], TSP‐2, and von Willebrand factor [vWF]). At EOS, seven markers were upregulated including Ang‐2, C‐reactive protein (CRP), intercellular adhesion molecule‐1 (ICAM‐1), IGFBP‐1, IL‐6, TSP‐2, and vascular cell adhesion molecule‐1 (VCAM‐1). A statistical trend was also seen for increases of VEGF‐A and placenta growth factor (PlGF) at EOS. Throughout treatment, sEnd levels significantly increased, an observation that was recapitulated in cultured endothelial cells. This is the first report of plasma‐based biomarkers in patients receiving TRC105. TRC105 treatment by C2D1 was associated with decreases in several angiogenic factors, including Ang‐2, PDGF isoforms, and VEGF isoforms, offering insight into the mechanisms underlying TRC105s anti‐angiogenic, antitumor function. Increases in sEnd were the most significant of all observed biomarker changes and may reflect direct drug effects. Additionally, biomarker changes in response to TRC105 are distinct from those seen in patients treated with VEGF‐targeting drugs, suggesting the possible utility of combining these two classes of angiogenesis inhibitors in patients.


Molecular Cancer Therapeutics | 2013

Abstract A2: Exploratory textural CT evaluation of the combination of TRC105 (anti-endoglin monoclonal antibody; MAb) and bevacizumab (BEV) indicates partial response by Choi criteria in BEV refractory advanced cancer patients (pts) and identifies candidate markers of response.

Ron L. Korn; Michael S. Gordon; Lee S. Rosen; Francisco Robert; Daniela Matei; Jonathan W. Goldman; David S. Mendelson; E. Gabriela Chiorean; Robert Matthew Strother; Ben K. Seon; Delia Alvarez; Bonne J. Adams; Charles P. Theuer

Background: Endoglin (CD105) is an endothelial cell membrane receptor, highly expressed on angiogenic tumor vessels, that is essential for angiogenesis and upregulated by hypoxia and VEGF inhibition. TRC105 is an anti-endoglin MAb that potentiates VEGF inhibitors in preclinical models. TRC105 10 mg/kg weekly was well tolerated with BEV 10 mg/kg q2wk and the combination demonstrated activity in BEV and VEGF TKI refractory pts. This study assessed radiographic responses to TRC105 + BEV using Choi criteria and tumor morphology by applying novel quantitative textural analysis (QTA: TexRad -University of Sussex, UK) in pts with durable stable disease by RECIST, to determine predictive markers of response. Methods: Contrast enhanced CT scans from 5 pts with advanced solid tumors who demonstrated stable disease by RECIST in a trial of escalating doses of TRC105 (3, 6, 8 or 10 mg/kg/wk) plus BEV were reviewed. Seventeen target lesions were selected from baseline scans and assessed for target lesion diameter, whole lesion density, and tumor volume at baseline and follow-up. QTA analysis was assessed on the same target lesions using six different filter levels at baseline and on follow-up scans. The results were correlated to anatomic tumor response using non-parametric evaluation and regression analysis. Statistical significance was defined as a two-tailed p < 0.05. Results: Scans from 5 patients (median age 56; M:F 2:3; median 4 prior regimens; 3 metastatic colorectal and 2 ovarian cancer) 4 of whom progressed following VEGF inhibitor treatment were selected and demonstrated stable disease by RECIST for at least 4 months (range: 4-14 months) of treatment with TRC105 + BEV. Four of five patients (80%) had partial responses by Choi criteria. Predictive markers of tumor response on baseline scans included 1) elevated mean pixel density (median values of responder (R) vs non responder (NR): 27.2 vs -4.3) that correlated with subsequent tumor size reduction, 2) elevated entropy (a measure of tumor heterogeneity; median R vs NR: 5.1 vs 4.7) that correlated with subsequent decrease in mean tumor volume, and 3) low kurtosis (a measure of tumor heterogeneity; median R vs NR: 0.2 vs 1.1) that correlated with subsequent reduction in lesion density (p<0.01). Mean positive pixel values (an indicator of hypoxia) on follow-up scans correlated with decreased tumor density. Conclusions: Assessment of radiographic response using Choi criteria identified VEGF inhibitor refractory patients who demonstrated partial response to the combination of TRC105 + BEV. Using novel QTA measures, markers of tumor heterogeneity and hypoxia correlated with individual lesion responses and are worthy of prospective evaluation as predictive imaging biomarkers. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):A2. Citation Format: Ron L. Korn, Michael S. Gordon, Lee S. Rosen, Francisco Robert, Daniela Matei, Jonathan W. Goldman, David S. Mendelson, E. Gabriela Chiorean, Robert Matthew Strother, Ben K. Seon, Delia Alvarez, Bonne J. Adams, Charles P. Theuer. Exploratory textural CT evaluation of the combination of TRC105 (anti-endoglin monoclonal antibody; MAb) and bevacizumab (BEV) indicates partial response by Choi criteria in BEV refractory advanced cancer patients (pts) and identifies candidate markers of response. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr A2.


Oncologist | 2018

An Open Label Phase Ib Dose Escalation Study of TRC105 (Anti‐Endoglin Antibody) with Axitinib in Patients with Metastatic Renal Cell Carcinoma

Toni K. Choueiri; M. Dror Michaelson; Edwin M. Posadas; Guru Sonpavde; David F. McDermott; Andrew B. Nixon; Yingmiao Liu; Zhenhua Yuan; Ben K. Seon; Meghara Walsh; Manoj A. Jivani; Bonne J. Adams; Charles P. Theuer

BACKGROUND TRC105 is an IgG1 endoglin monoclonal antibody that potentiates VEGF inhibitors in preclinical models. We assessed safety, pharmacokinetics, and antitumor activity of TRC105 in combination with axitinib in patients with metastatic renal cell carcinoma (mRCC). SUBJECTS, MATERIALS, AND METHODS Heavily pretreated mRCC patients were treated with TRC105 weekly (8 mg/kg and then 10 mg/kg) in combination with axitinib (initially at 5 mg b.i.d. and then escalated per patient tolerance to a maximum of 10 mg b.i.d.) until disease progression or unacceptable toxicity using a standard 3 + 3 phase I design. RESULTS Eighteen patients (median number of prior therapies = 3) were treated. TRC105 dose escalation proceeded to 10 mg/kg weekly without dose-limiting toxicity. Adverse event characteristics of each drug were not increased in frequency or severity when the two drugs were administered concurrently. TRC105 and axitinib demonstrated preliminary evidence of activity, including partial responses (PR) by RECIST in 29% of patients, and median progression-free survival (11.3 months). None of the patients with PR had PR to prior first-line treatment. Lower baseline levels of osteopontin and higher baseline levels of TGF-β receptor 3 correlated with overall response rate. CONCLUSION TRC105 at 8 and 10 mg/kg weekly was well tolerated in combination with axitinib, with encouraging evidence of activity in patients with mRCC. A multicenter, randomized phase II trial of TRC105 and axitinib has recently completed enrollment (NCT01806064). IMPLICATIONS FOR PRACTICE TRC105 is a monoclonal antibody to endoglin (CD105), a receptor densely expressed on proliferating endothelial cells and also on renal cancer stem cells that is implicated as a mediator of resistance to inhibitors of the VEGF pathway. In this Phase I trial, TRC105 combined safely with axitinib at the recommended single agent doses of each drug in patients with renal cell carcinoma. The combination demonstrated durable activity in a VEGF inhibitor-refractory population and modulated several angiogenic biomarkers. A randomized Phase II trial testing TRC105 in combination with axitinib in clear cell renal cell carcinoma has completed accrual.


Molecular Cancer Therapeutics | 2018

Modulation of Circulating Protein Biomarkers in Cancer Patients Receiving Bevacizumab and the Anti-Endoglin Antibody, TRC105

Yingmiao Liu; Mark D. Starr; John C. Brady; Christel Rushing; Herbert Pang; Bonne J. Adams; Delia Alvarez; Charles P. Theuer; Herbert Hurwitz; Andrew B. Nixon

TRC105 is an anti-endoglin antibody currently being tested in combination with VEGF inhibitors. In the phase Ib trial, 38 patients were treated with both TRC105 and bevacizumab (BEV), and improved clinical outcomes were observed, despite the fact that 30 patients (79%) were refractory to prior anti-VEGF therapy. Plasma samples were tested for angiogenic and inflammatory biomarkers at baseline and on-treatment. To provide broader context of this combination biomarker study, direct cross-study comparisons were made to biomarker studies previously conducted in patients treated with either BEV or TRC105 monotherapy. Upon treatment with BEV and TRC105, pharmacodynamic changes in response to both BEV (PlGF increase) and TRC105 (soluble endoglin increase) were noted. In addition, distinct patterns of change were identified (similar, opposing, neutralizing). Similar patterns were observed when the combination elicited similar effects to those observed with monotherapy treatment (i.e., decreases of Ang-2, increases of IL6 and VCAM-1). Opposing patterns were observed when the combination led to opposing effects compared with monotherapy treatment (i.e., TGFβ1, PDGF-AA and PDGF-BB, PAI-1). Lastly, neutralizing patterns were observed when one drug led to increase, whereas the other drug led to decrease, and the combination elicited no overall effect on the marker (i.e., VEGF-A, VEGF-D, and IGFBP-3). Patients achieving partial responses or stable disease from the combination exhibited significantly lower expression of E-Cadherin, HGF, ICAM-1, and TSP-2 at baseline. Taken together, the novel biomarker modulations identified may deepen our understanding of the underlying biology in patients treated with BEV and TRC105 compared with either drug alone. Mol Cancer Ther; 17(10); 2248–56. ©2018 AACR.


Cancer Research | 2014

Abstract CT222: Differences in pharmacokinetics of TRC105 (anti-endoglin antibody) when administered as a single agent versus in combination with bevacizumab (Bev)

Shawn D. Spencer; Lee S. Rosen; Michael S. Gordon; Francisco Robert; Daniela Matei; Cody J. Peer; Bonne J. Adams; Delia Alvarez; Ben K. Seon; Charles P. Theuer; W. Douglas Figg

Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA Background: TRC105 is an anti-endoglin chimeric monoclonal antibody that inhibits angiogenesis and tumor growth and is being studied in randomized Phase 2 trials with Bev. TRC105 is cleared through binding to endoglin expressed on proliferating endothelium when given as a single agent to cancer patients (Spencer et al, ASCO 2012). Preclinical data indicate that endoglin expression is increased in response to VEGF targeted treatment, and increased endoglin expression in response to Bev may increase the clearance of TRC105 when administered in combination to cancer patients. Methods: Patients (pts) with solid tumors (ST) or ovarian cancer (OC) received 10 mg/kg/wk TRC105 as a single agent, and additional patients with ST (primarily ovarian and colorectal) received 10 mg/kg/wk TRC105 with Bev. Peak and trough levels were assessed by ELISA in 39 patients who received TRC105 alone and compared to that of 35 patients (largely Bev refractory) who received TRC105 and Bev. Pts administered TRC105 and Bev were considered a population sub-group and treated as a covariate. A population pharmacokinetic model of TRC105 disposition was built using rich sampling from the ST trial, with sparse data from OC and TRC105+Bev included in the base model. A two-compartment model with nonlinear elimination best fit the data, utilizing Michaelis-Menten parameters for saturable clearance. Results: TRC105 peak and trough concentrations exceeded target serum concentrations of TRC105 known to saturate endoglin receptors in all pts dosed with 10 mg/kg/wk of TRC105 with and without Bev. The PK of TRC105 given with Bev had mean predicted (following 10,000 simulations) parameters of volume of distribution in the central compartment (VC), VMAX, and KM that were increased compared to population estimated parameters of TRC105 given as a single agent [VC= 44.5±2 (SE) (mL/kg) Pop mean estimate vs. 68.8±4 (mL/kg) Bev predicted; VMAX = 92.6±16 (μg/hr) vs. 297.5±40 (μg/hr) predicted, and KM= 5.91±2 (μg/mL) vs. 61.6±8.8 (μg/mL)]. All differences were significant (p<0.001). Observable data from patients administered the combination yielded PK parameters that were consistent with increased target-mediated clearance of TRC105 when given with Bev. Conclusions: Peak and trough TRC105 serum levels exceed target serum concentrations when given at 10 mg/kg/wk as a single agent or with Bev. Central compartment distribution of TRC105 increased when given with Bev, which is consistent with increased endoglin expression on proliferating endothelium following Bev treatment. The maximum rate of elimination (Vmax) also increased, consistent with increased turnover; however the intrinsic clearance ratio of Vmax/Km remained the same, suggesting no change in endoglin turnover efficiency. Future studies will assess whether PK parameters correlate with responses to the combination of TRC105 and Bev in Bev refractory patients. Citation Format: Shawn D. Spencer, Lee S. Rosen, Michael S. Gordon, Francisco Robert, Daniela Matei, Cody J. Peer, Bonne Adams, Delia Alvarez, Ben K. Seon, Charles P. Theuer, W. Douglas Figg. Differences in pharmacokinetics of TRC105 (anti-endoglin antibody) when administered as a single agent versus in combination with bevacizumab (Bev). [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr CT222. doi:10.1158/1538-7445.AM2014-CT222


Molecular Cancer Therapeutics | 2009

Abstract B62: A phase 1 study of oral TRC102 (methoxyamine), an inhibitor of base‐excision repair, to potentiate the therapeutic effects of pemetrexed in patients with advanced refractory cancer

Michael S. Gordon; Glen J. Weiss; Lee S. Rosen; David S. Mendelson; Ramesh K. Ramanathan; Jonathan W. Goldman; Bonne J. Adams; Delia Alvarez; Lili Liu; Stanton L. Gerson; Charles P. Theuer; Bryan R. Leigh

Background: TRC102 is a small molecule inhibitor of base‐excision repair (BER) that is highly water soluble and nearly completely bioavailable after oral administration. TRC102 potentiates the cytotoxicity of alkylator and antimetabolite chemotherapy and reverses chemotherapy resistance by rapidly and covalently binding to chemotherapy‐induced abasic sites. TRC102‐bound DNA is no longer a substrate for BER enzymes and is instead cleaved by topoisomerase II resulting in double‐strand breaks that trigger apoptosis. Methods: This Phase 1 trial evaluated the safety, PK, and PD of oral TRC102 combined with intravenous pemetrexed in patients with advanced refractory cancer. Patients were required to have ECOG PS ≤ 1 and adequate organ function. TRC102 was escalated in cohorts of 3–6 evaluable patients in combination with standard‐dose pemetrexed. All patients received TRC102 alone on Days 1–4 of a 2‐week cycle followed by the combination of TRC102 (D1–4) and pemetrexed (D1) every 3 weeks thereafter. Results: 20 patients were treated with a total of 65 cycles of TRC102 at 15 mg/m 2 (n=4), 30 mg/m 2 (n=7), 60 mg/m 2 (n=3) and 100 mg/m 2 (n=6). 18 of the 20 patients were evaluable for safety. No adverse events were attributed to TRC102 alone up to 60 mg/m 2 . One of six patients treated at 100 mg/m 2 experienced dose‐limiting Grade 3 anemia with TRC102 alone in Cycle 1. The patient remains on study in Cycle 3 with a 50% dose‐reduction of TRC102. Adverse events considered possibly related to the combination of TRC102 + pemetrexed included Grade 3–4 neutropenia without fever, Grade 3 thrombocytopenia, and Grade 1–2 fatigue and asthenia. The only other DLT was Grade 3 anemia in a patient who received 30 mg/m 2 TRC102 + pemetrexed in Cycle 2. The patient remained on study through Cycle 5 with a 50% dose‐reduction of TRC102. Clinical PK analyses indicated that TRC102 plasma concentrations required for in vivo activity were achieved with daily oral administration at all dose levels (C max > 50 ng/mL, t ½ > 24 hr). PD studies confirmed that TRC102 binds pemetrexed‐induced abasic sites in these patients. One patient with squamous cell carcinoma of the tonsillar fossa recurrent in the right lung and right hilum had RECIST‐defined partial response after 2 cycles of 30 mg/m 2 TRC102 + pemetrexed that is ongoing in Cycle 10. One patient with epithelial clear cell cancer of the ovary metastatic to the liver had a mixed response after 2 cycles of 30 mg/m 2 TRC102 + pemetrexed. Stable disease for 9 cycles was observed in a patient with metastatic squamous cell lung cancer at 30 mg/m 2 TRC102 + pemetrexed as 3rd line therapy. Conclusion: Daily oral TRC102 for 4 days is tolerated at doses that may potentiate the clinical activity of pemetrexed in patients with advanced refractory cancer. Phase 2 studies are planned in multiple indications. Citation Information: Mol Cancer Ther 2009;8(12 Suppl):B62.


Journal of Clinical Oncology | 2005

Phase II study of SU11248, a multitargeted receptor tyrosine kinase inhibitor (TKI), in patients (pts) with previously treated metastatic breast cancer (MBC)

Kathy D. Miller; Harold J. Burstein; Anthony Elias; Hope S. Rugo; Melody A. Cobleigh; Mark D. Pegram; P. D. Eisenberg; M. Collier; Bonne J. Adams; Charles M. Baum

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Charles P. Theuer

University of Wisconsin-Madison

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Lee S. Rosen

University of California

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Ben K. Seon

Roswell Park Cancer Institute

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Bryan R. Leigh

University of California

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Francisco Robert

University of Alabama at Birmingham

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Stanton L. Gerson

Case Western Reserve University

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