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Article ; Online: Efficacy of ganitumab (AMG 479), alone and in combination with rapamycin, in Ewing's and osteogenic sarcoma models.

Beltran, Pedro J / Chung, Young-Ah / Moody, Gordon / Mitchell, Petia / Cajulis, Elaina / Vonderfecht, Steven / Kendall, Richard / Radinsky, Robert / Calzone, Frank J

The Journal of pharmacology and experimental therapeutics

2011 Volume 337, Issue 3, Page(s) 644–654

Abstract: Ewing's and osteogenic sarcoma are two of the leading causes of cancer deaths in children and adolescents. Recent data suggest that sarcomas may depend on the insulin-like growth factor type 1 (IGF-1) receptor (IGF1R) and/or the insulin receptor (INSR) ... ...

Abstract	Ewing's and osteogenic sarcoma are two of the leading causes of cancer deaths in children and adolescents. Recent data suggest that sarcomas may depend on the insulin-like growth factor type 1 (IGF-1) receptor (IGF1R) and/or the insulin receptor (INSR) to drive tumor growth, survival, and resistance to mammalian target of rapamycin complex 1 (mTORC1) inhibitors. We evaluated the therapeutic value of ganitumab (AMG 479; C(6472)H(10028)N(1728)O(2020)S(42)), an anti-IGF1R, fully human monoclonal antibody, alone and in combination with rapamycin (mTORC1 inhibitor) in Ewing's (SK-ES-1 and A673) and osteogenic (SJSA-1) sarcoma models. IGF1R was activated by IGF-1 but not by insulin in each sarcoma model. INSR was also activated by IGF-1 in the SJSA-1 and SK-ES-1 models, but not in the A673 model where insulin was the preferred INSR ligand. Ganitumab significantly inhibited the growth of SJSA-1 and SK-ES-1 xenografts; inhibition was associated with decreased IGF1R and Akt phosphorylation, reduced total IGF1R and bromodeoxyuridine detection, and increased caspase-3 expression. Ganitumab inhibited rapamycin-induced IGF1R, Akt, and glycogen synthase kinase-3β hyperphosphorylation in each sarcoma model. However, ganitumab in combination with rapamycin also resulted in a marked increase in INSR expression and activity in the SJSA-1 and A673 models. The in vivo efficacy of ganitumab in the two ganitumab-sensitive models (SJSA-1 and SK-ES-1) was significantly enhanced in combination with rapamycin. Our results support studying ganitumab in combination with mTORC1 inhibitors for the treatment of sarcomas and suggest that INSR signaling is an important mechanism of resistance to IGF1R blockade.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/pharmacology ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Bone Neoplasms/drug therapy ; Bone Neoplasms/metabolism ; Caspase 3/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Female ; Humans ; Insulin-Like Growth Factor I/antagonists & inhibitors ; Insulin-Like Growth Factor I/metabolism ; Mice ; Mice, Nude ; Osteosarcoma/drug therapy ; Osteosarcoma/metabolism ; Phosphorylation/drug effects ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/antagonists & inhibitors ; Receptor, Insulin/metabolism ; Sarcoma, Ewing/drug therapy ; Sarcoma, Ewing/metabolism ; Signal Transduction/drug effects ; Sirolimus/pharmacology ; Sirolimus/therapeutic use ; Xenograft Model Antitumor Assays
Chemical Substances	AMG 479 ; Antibiotics, Antineoplastic ; Antibodies, Monoclonal ; Insulin-Like Growth Factor I (67763-96-6) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1) ; Caspase 3 (EC 3.4.22.-) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2011-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.110.178400
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Article ; Online: Ganitumab (AMG 479) inhibits IGF-II-dependent ovarian cancer growth and potentiates platinum-based chemotherapy.

Beltran, Pedro J / Calzone, Frank J / Mitchell, Petia / Chung, Young-Ah / Cajulis, Elaina / Moody, Gordon / Belmontes, Brian / Li, Chi-Ming / Vonderfecht, Steven / Velculescu, Victor E / Yang, Guorong / Qi, Jingwei / Slamon, Dennis J / Konecny, Gottfried E

Clinical cancer research : an official journal of the American Association for Cancer Research

2014 Volume 20, Issue 11, Page(s) 2947–2958

Abstract: Purpose: Insulin-like growth factor 1 receptor (IGF-IR) has been implicated in the pathogenesis of ovarian cancer. Ganitumab is an investigational, fully human monoclonal antibody against IGF-IR. Here, we explore the therapeutic potential of ganitumab ... ...

Abstract	Purpose: Insulin-like growth factor 1 receptor (IGF-IR) has been implicated in the pathogenesis of ovarian cancer. Ganitumab is an investigational, fully human monoclonal antibody against IGF-IR. Here, we explore the therapeutic potential of ganitumab for the treatment of ovarian cancer. Experimental design: The effects of ganitumab were tested in vitro against a panel of 23 established ovarian cancer cell lines. The ability of ganitumab to inhibit IGF-I-, IGF-II-, and insulin-mediated signaling was examined in vitro and in tumor xenografts using ovarian cancer models displaying IGF-IR/PI3K/AKT pathway activation by two distinct mechanisms, PTEN loss and IGF-II overexpression. Drug interactions between ganitumab and cisplatin, carboplatin, or paclitaxel were studied in vitro and in vivo. Results: In vitro, growth inhibition varied significantly among individual ovarian cancer cell lines. IGF-II mRNA and phospho-IGF-IR protein expression were quantitatively correlated with response to ganitumab, and PTEN mutations conferred resistance to ganitumab. Ganitumab potently inhibited baseline and IGF-I-, IGF-II-, and insulin-induced IGF-IR and IGF-IR/insulin hybrid receptor signaling in vitro and in vivo. Synergistic and additive drug interactions were seen for ganitumab and carboplatin or paclitaxel in vitro. Furthermore, ganitumab significantly increased the efficacy of cisplatin in ovarian cancer xenograft models in vivo. Conclusions: These observations provide a biologic rationale to test ganitumab as a single agent or in combination with carboplatin/cisplatin and paclitaxel in patients with ovarian cancer. Moreover, assessment of tumor expression of IGF-II, phospho-IGF-IR, or PTEN status may help select patients with ovarian cancer who are most likely to benefit from ganitumab. Clin Cancer Res; 20(11); 2947-58. ©2014 AACR.
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents/pharmacology ; Blotting, Western ; Carboplatin/administration & dosage ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cisplatin/administration & dosage ; Drug Synergism ; Female ; Flow Cytometry ; Humans ; Insulin-Like Growth Factor II/metabolism ; Mice ; Mice, Nude ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; PTEN Phosphohydrolase/genetics ; Paclitaxel/administration & dosage ; Receptor, IGF Type 1/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Transcriptome ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Insulin-Like Growth Factor II (67763-97-7) ; Carboplatin (BG3F62OND5) ; ganitumab (CK1441RCZ8) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Paclitaxel (P88XT4IS4D) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2014-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-13-3448
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Article ; Online: IGF1R blockade with ganitumab results in systemic effects on the GH-IGF axis in mice.

Moody, Gordon / Beltran, Pedro J / Mitchell, Petia / Cajulis, Elaina / Chung, Young-Ah / Hwang, David / Kendall, Richard / Radinsky, Robert / Cohen, Pinchas / Calzone, Frank J

The Journal of endocrinology

2014 Volume 221, Issue 1, Page(s) 145–155

Abstract: Ganitumab is a fully human MAB to the human type 1 IGF receptor (IGF1R). Binding assays showed that ganitumab recognized murine IGF1R with sub-nanomolar affinity (KD=0.22 nM) and inhibited the interaction of murine IGF1R with IGF1 and IGF2. Ganitumab ... ...

Abstract	Ganitumab is a fully human MAB to the human type 1 IGF receptor (IGF1R). Binding assays showed that ganitumab recognized murine IGF1R with sub-nanomolar affinity (KD=0.22 nM) and inhibited the interaction of murine IGF1R with IGF1 and IGF2. Ganitumab inhibited IGF1-induced activation of IGF1R in murine lungs and CT26 murine colon carcinoma cells and tumors. Addition of ganitumab to 5-fluorouracil resulted in enhanced inhibition of tumor growth in the CT26 model. Pharmacological intervention with ganitumab in naïve nude mice resulted in a number of physiological changes described previously in animals with targeted deletions of Igf1 and Igf1r, including inhibition of weight gain, reduced glucose tolerance and significant increase in serum levels of GH, IGF1 and IGFBP3. Flow cytometric analysis identified GR1/CD11b-positive cells as the highest IGF1R-expressing cells in murine peripheral blood. Administration of ganitumab led to a dose-dependent, reversible decrease in the number of peripheral neutrophils with no effect on erythrocytes or platelets. These findings indicate that acute IGF availability for its receptor plays a critical role in physiological growth, glucose metabolism and neutrophil physiology and support the presence of a pituitary IGF1R-driven negative feedback loop that tightly regulates serum IGF1 levels through Gh signaling.
MeSH term(s)	Animals ; Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Female ; Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor Binding Protein 3/metabolism ; Insulin-Like Growth Factor I/metabolism ; Insulin-Like Growth Factor II/metabolism ; Kinetics ; Lung/drug effects ; Lung/metabolism ; Male ; Mice ; Mice, Nude ; Phosphorylation/drug effects ; Receptor, IGF Type 1/antagonists & inhibitors ; Receptor, IGF Type 1/chemistry ; Receptor, IGF Type 1/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor I (67763-96-6) ; Insulin-Like Growth Factor II (67763-97-7) ; Growth Hormone (9002-72-6) ; ganitumab (CK1441RCZ8) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2014-03-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3028-4
ISSN	1479-6805 ; 0022-0795
ISSN (online)	1479-6805
ISSN	0022-0795
DOI	10.1530/JOE-13-0306
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Article ; Online: Epitope-specific mechanisms of IGF1R inhibition by ganitumab.

Calzone, Frank J / Cajulis, Elaina / Chung, Young-Ah / Tsai, Mei-Mei / Mitchell, Petia / Lu, John / Chen, Ching / Sun, Jilin / Radinsky, Robert / Kendall, Richard / Beltran, Pedro J

PloS one

2013 Volume 8, Issue 2, Page(s) e55135

Abstract: Background: Therapeutic antibodies targeting the IGF1R have shown diverse efficacy and safety signals in oncology clinical trials. The success of these agents as future human therapeutics depends on understanding the specific mechanisms by which these ... ...

Abstract	Background: Therapeutic antibodies targeting the IGF1R have shown diverse efficacy and safety signals in oncology clinical trials. The success of these agents as future human therapeutics depends on understanding the specific mechanisms by which these antibodies target IGF1R signaling. Methodology/principal findings: A panel of well-characterized assays was used to investigate the mechanisms by which ganitumab, a fully human anti-IGF1R antibody undergoing clinical testing, inhibits IGF1R activity. Epitope mapping using IGF1R subdomains localized the ganitumab binding site to the L2 domain. Binding of ganitumab inhibited the high-affinity interaction of IGF-1 and IGF-2 required to activate IGF1R in cells engineered for IGF1R hypersensitivity and in human cancer cell lines, resulting in complete blockade of ligand-induced cellular proliferation. Inhibition of IGF1R activity by ganitumab did not depend on endosomal sequestration, since efficient ligand blockade was obtained without evidence of receptor internalization and degradation. Clinically relevant concentrations of ganitumab also inhibited the activation of hybrid receptors by IGF-1 and IGF-2. Ganitumab was not an agonist of homodimeric IGF1R or hybrid receptors in MCF-7 and COLO 205 cells, but low-level IGF1R activation was detected in cells engineered for IGF1R hypersensitivity. This activation seems biologically irrelevant since ganitumab completely inhibited ligand-driven proliferation. The in vivo efficacy profile of ganitumab was equivalent or better than CR and FnIII-1 domain-specific antibodies, alone or in combination with irinotecan. CR domain-specific antibodies only blocked IGF-1 binding to IGF1R but were more potent than ganitumab at inducing homodimer and hybrid receptor downregulation in vitro, however this difference was less obvious in vivo. No inhibition of hybrid receptors was observed with the FnIII-1 domain antibodies, which were relatively strong homodimer and hybrid agonists. Conclusions/significance: The safety and efficacy profile of ganitumab and other anti-IGF1R antibodies may be explained by the distinct molecular mechanisms by which they inhibit receptor signaling.
MeSH term(s)	Analysis of Variance ; Animals ; Antibodies, Monoclonal/metabolism ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Antibody Affinity ; Binding Sites/genetics ; Cell Proliferation ; Epitope Mapping ; Female ; Humans ; Insulin-Like Growth Factor I/metabolism ; Insulin-Like Growth Factor II/metabolism ; MCF-7 Cells ; Mice ; Mice, Nude ; Phosphorylation ; Receptor, IGF Type 1/antagonists & inhibitors ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Insulin-Like Growth Factor I (67763-96-6) ; Insulin-Like Growth Factor II (67763-97-7) ; ganitumab (CK1441RCZ8) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2013-02-01
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0055135
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Article ; Online: Discovery of 1H-pyrazol-3(2H)-ones as potent and selective inhibitors of protein kinase R-like endoplasmic reticulum kinase (PERK).

Journal of medicinal chemistry

2015 Volume 58, Issue 3, Page(s) 1426–1441

Abstract: The structure-based design and optimization of a novel series of selective PERK inhibitors are described resulting in the identification of 44 as a potent, highly selective, and orally active tool compound suitable for PERK pathway biology exploration ... ...

Abstract	The structure-based design and optimization of a novel series of selective PERK inhibitors are described resulting in the identification of 44 as a potent, highly selective, and orally active tool compound suitable for PERK pathway biology exploration both in vitro and in vivo.
MeSH term(s)	Animals ; Cells, Cultured ; Dose-Response Relationship, Drug ; Drug Discovery ; Humans ; Mice ; Mice, Nude ; Models, Molecular ; Molecular Structure ; Protein Kinase Inhibitors/chemical synthesis ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Pyrazoles/chemical synthesis ; Pyrazoles/chemistry ; Pyrazoles/pharmacology ; Structure-Activity Relationship ; eIF-2 Kinase/antagonists & inhibitors ; eIF-2 Kinase/metabolism
Chemical Substances	Protein Kinase Inhibitors ; Pyrazoles ; EIF2AK3 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
Language	English
Publishing date	2015-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/jm5017494
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Article ; Online: HER-2 overexpression differentially alters transforming growth factor-beta responses in luminal versus mesenchymal human breast cancer cells.

Wilson, Cindy A / Cajulis, Elaina E / Green, Jennifer L / Olsen, Taylor M / Chung, Young Ah / Damore, Michael A / Dering, Judy / Calzone, Frank J / Slamon, Dennis J

Breast cancer research : BCR

2005 Volume 7, Issue 6, Page(s) R1058–79

Abstract: Introduction: Amplification of the HER-2 receptor tyrosine kinase has been implicated in the pathogenesis and aggressive behavior of approximately 25% of invasive human breast cancers. Clinical and experimental evidence suggest that aberrant HER-2 ... ...

Abstract	Introduction: Amplification of the HER-2 receptor tyrosine kinase has been implicated in the pathogenesis and aggressive behavior of approximately 25% of invasive human breast cancers. Clinical and experimental evidence suggest that aberrant HER-2 signaling contributes to tumor initiation and disease progression. Transforming growth factor beta (TGF-beta) is the dominant factor opposing growth stimulatory factors and early oncogene activation in many tissues, including the mammary gland. Thus, to better understand the mechanisms by which HER-2 overexpression promotes the early stages of breast cancer, we directly assayed the cellular and molecular effects of TGF-beta1 on breast cancer cells in the presence or absence of overexpressed HER-2. Methods: Cell proliferation assays were used to determine the effect of TGF-beta on the growth of breast cancer cells with normal or high level expression of HER-2. Affymetrix microarrays combined with Northern and western blot analysis were used to monitor the transcriptional responses to exogenous TGF-beta1 in luminal and mesenchymal-like breast cancer cells. The activity of the core TGF-beta signaling pathway was assessed using TGF-beta1 binding assays, phospho-specific Smad antibodies, immunofluorescent staining of Smad and Smad DNA binding assays. Results: We demonstrate that cells engineered to over-express HER-2 are resistant to the anti-proliferative effect of TGF-beta1. HER-2 overexpression profoundly diminishes the transcriptional responses induced by TGF-beta in the luminal MCF-7 breast cancer cell line and prevents target gene induction by a novel mechanism that does not involve the abrogation of Smad nuclear accumulation, DNA binding or changes in c-myc repression. Conversely, HER-2 overexpression in the context of the mesenchymal MDA-MB-231 breast cell line potentiated the TGF-beta induced pro-invasive and pro-metastatic gene signature. Conclusion: HER-2 overexpression promotes the growth and malignancy of mammary epithelial cells, in part, by conferring resistance to the growth inhibitory effects of TGF-beta. In contrast, HER-2 and TGF-beta signaling pathways can cooperate to promote especially aggressive disease behavior in the context of a highly invasive breast tumor model.
MeSH term(s)	Blotting, Northern ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Proliferation ; Disease Progression ; Epithelial Cells ; Female ; Gene Expression Profiling ; Genetic Engineering ; Humans ; Mammary Glands, Human/cytology ; Mesoderm ; Neoplasm Invasiveness ; Receptor, ErbB-2/biosynthesis ; Signal Transduction ; Transforming Growth Factor beta/physiology ; Transforming Growth Factor beta1
Chemical Substances	TGFB1 protein, human ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2005
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/bcr1343
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Article ; Online: Efficacy of ganitumab (AMG 479), alone and in combination with rapamycin, in Ewing's and osteogenic sarcoma models.

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Article ; Online: Ganitumab (AMG 479) inhibits IGF-II-dependent ovarian cancer growth and potentiates platinum-based chemotherapy.

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Article ; Online: IGF1R blockade with ganitumab results in systemic effects on the GH-IGF axis in mice.

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Article ; Online: Epitope-specific mechanisms of IGF1R inhibition by ganitumab.

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Article ; Online: Discovery of 1H-pyrazol-3(2H)-ones as potent and selective inhibitors of protein kinase R-like endoplasmic reticulum kinase (PERK).

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Article ; Online: HER-2 overexpression differentially alters transforming growth factor-beta responses in luminal versus mesenchymal human breast cancer cells.

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