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  • American Association for Cancer Research (AACR)  (8)
  • 1
    Online Resource
    Online Resource
    AMG 706, an Oral, Multikinase Inhibitor that Selectively Targets Vascular Endothelial Growth Factor, Platelet-Derived Growth Factor, and Kit Receptors, Potently Inhibits Angiogenesis and Induces Regression in Tumor Xenografts
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Research Vol. 66, No. 17 ( 2006-09-01), p. 8715-8721
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 17 ( 2006-09-01), p. 8715-8721
    Abstract: The growth of solid tumors is dependent on the continued stimulation of endothelial cell proliferation and migration resulting in angiogenesis. The angiogenic process is controlled by a variety of factors of which the vascular endothelial growth factor (VEGF) pathway and its receptors play a pivotal role. Small-molecule inhibitors of VEGF receptors (VEGFR) have been shown to inhibit angiogenesis and tumor growth in preclinical models and in clinical trials. A novel nicotinamide, AMG 706, was identified as a potent, orally bioavailable inhibitor of the VEGFR1/Flt1, VEGFR2/kinase domain receptor/Flk-1, VEGFR3/Flt4, platelet-derived growth factor receptor, and Kit receptors in preclinical models. AMG 706 inhibited human endothelial cell proliferation induced by VEGF, but not by basic fibroblast growth factor in vitro, as well as vascular permeability induced by VEGF in mice. Oral administration of AMG 706 potently inhibited VEGF-induced angiogenesis in the rat corneal model and induced regression of established A431 xenografts. AMG 706 was well tolerated and had no significant effects on body weight or on the general health of the animals. Histologic analysis of tumor xenografts from AMG 706–treated animals revealed an increase in endothelial apoptosis and a reduction in blood vessel area that preceded an increase in tumor cell apoptosis. In summary, AMG 706 is an orally bioavailable, well-tolerated multikinase inhibitor that is presently under clinical investigation for the treatment of human malignancies. (Cancer Res 2006; 66(17): 8715-21)
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-05-4665
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
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  • 2
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    Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody
    American Association for Cancer Research (AACR) ; 2010
    In:  Molecular Cancer Therapeutics Vol. 9, No. 10 ( 2010-10-01), p. 2641-2651
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 9, No. 10 ( 2010-10-01), p. 2641-2651
    Abstract: AMG 386 is an investigational first-in-class peptide-Fc fusion protein (peptibody) that inhibits angiogenesis by preventing the interaction of angiopoietin-1 (Ang1) and Ang2 with their receptor, Tie2. Although the therapeutic value of blocking Ang2 has been shown in several models of tumorigenesis and angiogenesis, the potential benefit of Ang1 antagonism is less clear. To investigate the consequences of Ang1 neutralization, we have developed potent and selective peptibodies that inhibit the interaction between Ang1 and its receptor, Tie2. Although selective Ang1 antagonism has no independent effect in models of angiogenesis-associated diseases (cancer and diabetic retinopathy), it induces ovarian atrophy in normal juvenile rats and inhibits ovarian follicular angiogenesis in a hormone-induced ovulation model. Surprisingly, the activity of Ang1 inhibitors seems to be unmasked in some disease models when combined with Ang2 inhibitors, even in the context of concurrent vascular endothelial growth factor inhibition. Dual inhibition of Ang1 and Ang2 using AMG 386 or a combination of Ang1- and Ang2-selective peptibodies cooperatively suppresses tumor xenograft growth and ovarian follicular angiogenesis; however, Ang1 inhibition fails to augment the suppressive effect of Ang2 inhibition on tumor endothelial cell proliferation, corneal angiogenesis, and oxygen-induced retinal angiogenesis. In no case was Ang1 inhibition shown to (a) confer superior activity to Ang2 inhibition or dual Ang1/2 inhibition or (b) antagonize the efficacy of Ang2 inhibition. These results imply that Ang1 plays a context-dependent role in promoting postnatal angiogenesis and that dual Ang1/2 inhibition is superior to selective Ang2 inhibition for suppression of angiogenesis in some postnatal settings. Mol Cancer Ther; 9(10); 2641–51. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-10-0213
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    SSG: 12
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  • 3
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    Abstract 1608: Angiopoietin 2 is elevated in patients with RCC, and Ang2 inhibition improves antiantiogenic activity of sunitinib in a mouse model of RCC.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1608-1608
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1608-1608
    Abstract: Background: Several small molecules targeting angiogenic receptor tyrosine kinases (TKIs) are approved for treatment of advanced RCC. While many patients (pts) respond to TKIs, resistance develops in all. Ang2 is a secreted glycoprotein that is upregulated at sites of angiogenesis and has been implicated in cancer neovascularization. Ang2 is elevated in many cancer states, and higher levels are associated with poor prognosis. Recent studies have also suggested efficacy of combined Ang and VEGFR inhibition as therapy in RCC. Mehtods: A panel of angiogenic genes was analyzed by RT-PCR in several tumor vs normal tissues. Plasma Ang2 levels in pts with RCC were measured in duplicate at baseline, on treatment with sunitinib (median 34.5 days after starting sunitinib), and at resistance to sunitinib. Finally, dual Ang1/2 (AMG 386) or Ang2 (L1-7) inhibition was also tested in a murine RCC xenograft model of resistance to VEGFR inhibition. Tumors were assessed for blood flow by arterial spin labeled (ASL) MRI. Results: Among the genes studied, Ang2 levels were 6.7 fold higher in human tumors vs normal (nl) tissues, and 12.6 fold higher in RCC vs nl. RCC ranked highest for Ang2 expression across all the tumor types tested, with Ang2 levels in RCC being 2.8 fold higher than in all other tumor types. VEGF and KDR showed similar results, with both exhibiting higher levels in tumors vs nl tissues (7.5 fold for VEGF and 2 fold for KDR). VEGF was 25.5 fold higher in RCC vs nl, and KDR was 6 fold higher in RCC vs nl. VEGF and KDR were also higher in RCC than all other tumor types (7.0 fold for VEGF and 6.5 fold for KDR). Plasma Ang2 was significantly higher in pts with metastatic RCC (n=50) compared to controls (n=26) and pts with stage I disease (n=39) (P & lt;0.001). Ang2 was also measured in pts at baseline, day 28 and at time of progression on sunitinib. Plasma Ang2 decreased at day 28 (n=39 pairs) and increased at the time of disease progression (n=28 pairs) (P & lt;0.001). In our mouse model of RCC, dual Ang1/2 (AMG 386) or Ang2 (L1-7) inhibition improved the activity of sunitinib (su) (time to progression on su, su+AMG 386, su+L1-7 = 25.6±12.4, 48.2±13.5, or 51.9±17.2 days, respectively (P & lt;0.05). Treatment with these agents exhibited a trend towards reduction in residual viable tissue after combination treatment and prevented the resumption of blood flow as measured with ASL MRI with sunitinib alone (tumor perfusion on day 50 post-treatment with su, su+AMG 386, su+L1-7 = 36.7±15.0, 18.4±11.1, or 16.0±7.3 ml/100g/min, respectively, P & lt;0.01). Conclusion: Ang2 inhibition is elevated in pts with RCC, and Ang2 inhibition improves the activity of sunitinib in our mouse model of resistance. Plasma Ang2 levels increase in pts treated with sunitinib and may contribute to resistance to therapy. It is possible that the subset of pts with the highest Ang2 at resistance may be the optimal candidates for combination of these antiangiogenic agents. Citation Format: Xiaoen Wang, Andrea Bullock, Liang Zhang, Dongyin Yu, Lin Wei, Jiaxi Song, Manoj Bhasin, Sabina Signoretti, David C. Alsop, James W. Mier, Michael B. Atkins, Angela Coxon, Jon Oliner, Rupal S. Bhatt. Angiopoietin 2 is elevated in patients with RCC, and Ang2 inhibition improves antiantiogenic activity of sunitinib in a mouse model of RCC. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1608. doi:10.1158/1538-7445.AM2013-1608
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-1608
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 4
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    Broad Antitumor Activity in Breast Cancer Xenografts by Motesanib, a Highly Selective, Oral Inhibitor of Vascular Endothelial Growth Factor, Platelet-Derived Growth Factor, and Kit Receptors
    American Association for Cancer Research (AACR) ; 2009
    In:  Clinical Cancer Research Vol. 15, No. 1 ( 2009-01-01), p. 110-118
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 15, No. 1 ( 2009-01-01), p. 110-118
    Abstract: Purpose: Angiogenesis plays a critical role in breast cancer development and progression. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor that regulates endothelial cell proliferation and survival. We investigated the effects of motesanib, a novel, oral inhibitor of VEGF receptors 1, 2, and 3; platelet-derived growth factor receptor; and Kit receptor, on the growth of xenografts representing various human breast cancer subtypes. Experimental Design: Athymic nude mice were implanted with MCF-7 (luminal) or MDA-MB-231 (mesenchymal) tumor fragments or Cal-51 (mixed/progenitor) tumor cells. Once tumors were established, animals were randomized to receive increasing doses of motesanib alone or motesanib plus cytotoxic chemotherapy (docetaxel, doxorubicin, or tamoxifen). Results: Across all three xenograft models, motesanib treatment resulted in significant dose-dependent reductions in tumor growth, compared with vehicle-treated controls, and in marked reductions in viable tumor fraction and blood vessel density. No significant effect on body weight was observed with compound treatment compared with control-treated animals. Motesanib did not affect the proliferation of tumor cells in vitro. There was a significantly greater reduction in xenograft tumor growth when motesanib was combined with docetaxel (MDA-MB-231 tumors) or with the estrogen receptor modulator tamoxifen (MCF-7 tumors), compared with either treatment alone, but not when combined with doxorubicin (Cal-51 tumors). Conclusions: Treatment with motesanib alone or in combination with chemotherapy inhibits tumor growth in vivo in various models of human breast cancer. These data suggest that motesanib may have broad utility in the treatment of human breast cancer.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-08-1155
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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  • 5
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    Abstract 5089: Combined treatment of trebananib (AMG 386) with panitumumab in preclinical tumor models.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 5089-5089
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 5089-5089
    Abstract: Introduction: Cancer therapies that combine agents directly targeting tumor cells with those impacting the tumor stroma hold the promise of improving patient outcomes. In this preclinical study, we examined the effects of inhibiting both EGF signaling in human tumor cells and angiopoietin signaling in the murine stroma. Using tumor xenograft models, we tested a treatment combination of panitumumab, a fully human monoclonal antibody against human EGF receptor, and trebananib, an investigational peptide-Fc fusion protein that prevents binding of angiopoietins 1 and 2 to their receptor, Tie2. We assessed the effect of this combination on tumor growth and explored mechanisms of enhanced efficacy. Methods: Athymic nude mice were injected SC in the right flank with either 1x107 A431 (human epidermoid carcinoma) or 5x106 DLD-1 (colon adenocarcinoma) cells. When tumors were ∼ 200 mm3, 20 μg panitumumab IP and/or 70 μg trebananib SC were given twice weekly. Controls were isotype antibody or human Fc. In mechanism of action studies, DLD-1 tumors (∼ 300-400 mm3) received 2 treatments over 5 days before harvest and processing for paraffin sectioning. To examine endothelial cell proliferation, treated tumors were enzyme-digested and stained with anti-CD31, anti-CD45, and anti-BrdU antibodies. The percentage of BrdU-positive tumor-associated endothelial cells (CD31high/CD45neg) was determined by flow cytometry. Results: In both tumor models, combined treatment with panitumumab and trebananib resulted in significantly greater tumor growth inhibition (p≤0.014) than treatment with either single agent alone. All treatments were well tolerated; no significant weight loss was observed. Mechanistic studies revealed that combination treatment did not alter the single-agent activity of either treatment: histological analyses showed a significant reduction in estimated blood vessel area within viable tumor after treatment with either trebananib (p=0.0006) or panitumumab (p=0.012) alone; this reduction was not affected by combination treatment. Similarly, BrdU incorporation assays demonstrated that single-agent panitumumab significantly impaired tumor cell proliferation (p=0.0003), whereas single-agent trebananib significantly reduced endothelial cell proliferation (p & lt;0.0001). Combined treatment did not change the effects on cell proliferation seen with either single agent alone. Conclusions: This study demonstrates that combined treatment with agents targeting EGF signaling in the tumor and angiopoietin signaling in the stroma results in significantly enhanced antitumor activity. Neither agent appears to impact the biochemical activities of the other, but instead gives rise to an orthogonal enhancement of antitumor activities. These findings support further clinical testing of agents that target the tumor stroma in combination with direct tumor-targeting therapies. Citation Format: James V. Bready, Paula Kaplan-Lefko, Jodi Moriguchi, Marc Payton, Stephen Kaufman, Jonathan Oliner, Robert Radinsky, Angela Coxon. Combined treatment of trebananib (AMG 386) with panitumumab in preclinical tumor models. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5089. doi:10.1158/1538-7445.AM2013-5089
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-5089
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 6
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    Complementary Actions of Inhibitors of Angiopoietin-2 and VEGF on Tumor Angiogenesis and Growth
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 6 ( 2010-03-15), p. 2213-2223
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 6 ( 2010-03-15), p. 2213-2223
    Abstract: Inhibition of angiopoietin-2 (Ang2) can slow tumor growth, but the underlying mechanism is not fully understood. Because Ang2 is expressed in growing blood vessels and promotes angiogenesis driven by vascular endothelial growth factor (VEGF), we asked whether the antitumor effect of Ang2 inhibition results from reduced sprouting angiogenesis and whether the effect is augmented by inhibition of VEGF from tumor cells. Using Colo205 human colon carcinomas in nude mice as a model, we found that selective inhibition of Ang2 by the peptide-Fc fusion protein L1-7(N) reduced the number of vascular sprouts by 46% and tumor growth by 62% over 26 days. Strikingly, when the Ang2 inhibitor was combined with a function-blocking anti-VEGF antibody, the number of sprouts was reduced by 82%, tumor vascularity was reduced by 67%, and tumor growth slowed by 91% compared with controls. The reduction in tumor growth was accompanied by decreased cell proliferation and increased apoptosis. We conclude that inhibition of Ang2 slows tumor growth by limiting the expansion of the tumor vasculature by sprouting angiogenesis, in a manner that is complemented by concurrent inhibition of VEGF and leads to reduced proliferation and increased apoptosis of tumor cells. Cancer Res; 70(6); 2213–23
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-1977
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
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    Abstract 494: Evaluation of soluble FLT3 ligand as a marker of bone marrow stress and recovery
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 494-494
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 494-494
    Abstract: Depletion of bone marrow (BM)-resident myeloid progenitor cells is a consequence of various anti-cancer treatments, including bispecific T-cell engager (BiTE®) antibodies targeting myeloid cell antigens. Currently, aspirates are required to determine the extent of myeloid cell depletion in the BM. This procedure is painful and potentially invasive for patients. As a surrogate marker for BM myeloid cell depletion, we evaluated soluble FLT3 ligand (FLT3L) in non-human primates treated with myeloid cell-depleting BiTE® antibodies. While FLT3L is not detectable in serum during steady-state hematopoiesis, it is detectable in response to hematopoietic deficiency. The goal of this study was to evaluate the relationship of serum FLT3L with depletion and recovery of BM myeloid cells in non-human primates treated with BiTE® antibodies against CD33. Serum FLT3L levels were determined using an anti-human FLT3L ELISA kit. Validation studies demonstrated that both the capture and detection antibodies recognized cynomolgus FLT3L. Serum FLT3L concentrations were determined using a standard curve with rhesus FLT3L (99.6% identical to cynomolgus FLT3L). Serum samples were taken from cynomolgus monkeys before, during and after treatment with anti-CD33 BiTE® antibodies and compared with the number of BM-resident target cells. In the first study, cynomolgus monkeys were dosed once with different dose levels of anti-CD33 BiTE® antibody ranging from 1- 15 μg/kg. BM-resident myeloid cells were transiently reduced in some, but not all, cohorts. Soluble FLT3L was detected only when there was a reduction in BM myeloid cells. When FLT3L was detectable, the serum concentration correlated with the extent of target cell reduction and FLT3L levels decreased as the myeloid cells recovered. In the second study, cynomolgus monkeys were dosed three times with anti-CD33 BiTE® antibody. In these studies target cell reduction was greater and persisted longer compared to the single dose studies. Similarly, the magnitude and duration of increased FLT3L in the multidose studies was also greater. Within the multi-dose study, FLT3L levels continued to increase as more BM-resident myeloid cells were depleted, suggesting that it was possible to detect cumulative stress to the BM. In summary, serum FLT3L levels are correlated with the extent and duration of myeloid cell depletion in the BM suggesting that serum FLT3L levels reflect depletion and subsequent myeloid cell replenishment. All studies to date have involved treatment with myeloid antigen-specific BiTE® antibodies; future studies will evaluate FLT3L levels following treatment with anti-lymphoid or solid tumor antigen-specific BiTE® antibodies to determine if FLT3L increases are associated with myeloid cell depletion or indicative of general BM stress or inflammation. The potential benefit of this marker is that it could allow for repeat non-invasive BM monitoring in patients on myelosuppressive therapies. Citation Format: Christine Sastri, Mercedesz Balazs, Priya Koppikar, James R. Lipford, Angela Coxon, Tara L. Arvedson. Evaluation of soluble FLT3 ligand as a marker of bone marrow stress and recovery. [abstract] . In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 494.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-494
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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    detail.hit.zdb_id: 410466-3
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  • 8
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    Abstract 1022: Development and preclinical testing of AMG 780, a fully human antibody targeting angiopoietin 1 (Ang1) and angiopoietin 2 (Ang2)
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1022-1022
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1022-1022
    Abstract: Targeting the angiopoietins with trebananib (a peptibody that inhibits the interaction between the endothelial cell-selective Tie2 receptor and its ligands Ang1 and Ang2) in combination with paclitaxel was associated with clinical benefit in a phase 3 ovarian cancer clinical trial (TRINOVA 1). Herein, we describe the generation of AMG 780, a fully human IgG2 antibody targeting Ang1 and Ang2. We compared AMG 780 to trebananib in affinity/neutralization ELISA assays and in vivo studies assessing inhibition of tumor growth and endothelial cell proliferation. AMG 780 is a derivative of an Ang2-binding antibody (Ab X). Ab X was generated by panning a human phage display Fab library (Dyax Corporation) against recombinant Ang2. The Ab X Fab was affinity matured by individually substituting every possible amino acid at every position in the light and heavy chain complementarity determining regions (CDRs). Resulting phage clones were interrogated for improved Ang1- and Ang2-binding activity. Clones with improved potency were converted to full antibodies. The most improved heavy chain clones were paired with the most improved light chain clones. The resulting IgGs were tested for neutralization of the interaction between the angiopoietins and their receptor, Tie2, as measured by homogenous time-resolved fluorescence (HTRF). Three resulting fully human IgG2 antibodies (AMG 780, Ab Y, and Ab Z) and the parental clone (Ab X) with potent Ang2 inhibitory activities (IC50 [nM], 0.05-0.10) and a range of Ang1 inhibitory activities (IC50 [nM] , 0.31-547.00) were selected for xenograft studies. Mice were implanted with 5x106 Colo205 (human colon carcinoma) cells. When tumors were approximately 200 mm3, 300 µg of each of the four antibodies intraperitoneally or 14 µg of trebananib subcutaneously were administered twice weekly. For viable tumor fraction analyses, treated tumors at the end of the xenograft study were harvested and processed for paraffin histology. To examine endothelial cell proliferation, treated tumors were enzyme digested and stained with anti-CD31, anti-CD45, and anti-BrdU antibodies. The percentage of BrdU-positive tumor-associated endothelial cells (CD31high/CD45neg) was determined by flow cytometry. Relative to an isotope control antibody, all four IgG2 antibodies and trebananib inhibited tumor growth (P & lt; 0.0001), viable tumor fraction (P & lt; 0.0001), and tumor endothelial cell proliferation (P & lt; 0.002). Tumor xenografts in those animals receiving AMG 780 exhibited the most pronounced inhibition in tumor growth (66%), viable tumor fraction (81%), and endothelial cell proliferation (84%). The inhibitory activities of AMG 780 (IC50 [nM]: Ang1, 4.5; Ang2, 0.06) were similar to those of trebananib (IC50 [nM] : Ang1, 3.5; Ang2, 0.03). Based on these findings, AMG 780 was selected for clinical development and currently is being evaluated in a first-in-human phase 1 trial. Citation Format: James V. Bready, Kyung Lee, Rick Jacobsen, Kevin Graham, Juan Estrada, Stephen A. Kaufman, Dongyin Yu, Angela Coxon, Jon Oliner. Development and preclinical testing of AMG 780, a fully human antibody targeting angiopoietin 1 (Ang1) and angiopoietin 2 (Ang2). [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 1022. doi:10.1158/1538-7445.AM2014-1022
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-1022
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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