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<script type="text/javascript" src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.boots.min.js"> </script><title>89Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody) - Molecular Imaging and Contrast Agent Database (MICAD) - NCBI Bookshelf</title>
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<meta name="citation_inbook_title" content="Molecular Imaging and Contrast Agent Database (MICAD) [Internet]">
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<meta name="citation_title" content="89Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody)">
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<meta name="citation_date" content="2012/01/26">
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<meta name="citation_author" content="Arvind Chopra">
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<meta name="DC.Title" content="89Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody)">
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<meta name="DC.Contributor" content="Arvind Chopra">
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<meta name="description" content="The transforming growth factor-β (TGF-β) belongs to a superfamily of cytokines that mediate their activity through serine/threonine kinase receptors and are involved in a variety of cellular processes such as proliferation, differentiation, and migration (1, 2). The TGF-β is a tumor suppressor, but under certain cellular conditions it can promote tumor progression and cancer metastasis as discussed by Meulmeester and ten Dijke (2) and Inman (3). Although TGF-β and its receptors are considered to be important targets for the treatment of highly invasive tumors such as glioblastomas and those of breast cancer, no drug or antibody is available to inhibit the activity of this cytokine or its receptor signaling pathway to treat these malignancies (4). A subset of breast cancer patients exhibited overexpression or suppression of genes related to the TGF-β signaling pathway, and these individuals also showed a shorter metastasis-free or relapse-free survival (5). Therefore, noninvasive imaging of TGF-β will not only help in understanding the functioning of this receptor–ligand system and assist in the development of novel agents that can target the TGF-β or its receptor, but it will also assist in the selection of patients who would benefit most from such an anti-cancer treatment (5).">
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<meta name="og:description" content="The transforming growth factor-β (TGF-β) belongs to a superfamily of cytokines that mediate their activity through serine/threonine kinase receptors and are involved in a variety of cellular processes such as proliferation, differentiation, and migration (1, 2). The TGF-β is a tumor suppressor, but under certain cellular conditions it can promote tumor progression and cancer metastasis as discussed by Meulmeester and ten Dijke (2) and Inman (3). Although TGF-β and its receptors are considered to be important targets for the treatment of highly invasive tumors such as glioblastomas and those of breast cancer, no drug or antibody is available to inhibit the activity of this cytokine or its receptor signaling pathway to treat these malignancies (4). A subset of breast cancer patients exhibited overexpression or suppression of genes related to the TGF-β signaling pathway, and these individuals also showed a shorter metastasis-free or relapse-free survival (5). Therefore, noninvasive imaging of TGF-β will not only help in understanding the functioning of this receptor–ligand system and assist in the development of novel agents that can target the TGF-β or its receptor, but it will also assist in the selection of patients who would benefit most from such an anti-cancer treatment (5).">
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id="jr-fip-info-p"><a id="jr-fip-prev" class="wsprkl btn" title="Jump to previuos match">◀</a><button id="jr-fip-matches">no matches yet</button><a id="jr-fip-next" class="wsprkl btn" title="Jump to next match">▶</a></nav></nav></div><div id="jr-epub-interstitial" class="hidden"></div><div id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK83581_"><span class="title" itemprop="name"><sup>89</sup>Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody)</span></h1><div itemprop="alternativeHeadline" class="subtitle whole_rhythm"> [<sup>89</sup>Zr]-Fresolimumab</div><p class="contribs">Chopra A.</p><p class="fm-aai"><a href="#_NBK83581_pubdet_">Publication Details</a></p></div></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div class="iconblock whole_rhythm clearfix ten_col table-wrap" id="figFresolimumab89ZrTncchemicalname89zrl"><a href="/books/NBK83581/table/Fresolimumab89Zr.T.nc_chemical_name89zrl/?report=objectonly" target="object" title="Table" class="img_link icnblk_img figpopup" rid-figpopup="figFresolimumab89ZrTncchemicalname89zrl" rid-ob="figobFresolimumab89ZrTncchemicalname89zrl"><img class="small-thumb" src="/books/NBK83581/table/Fresolimumab89Zr.T.nc_chemical_name89zrl/?report=thumb" src-large="/books/NBK83581/table/Fresolimumab89Zr.T.nc_chemical_name89zrl/?report=previmg" alt="Image " /></a><div class="icnblk_cntnt"><h4 id="Fresolimumab89Zr.T.nc_chemical_name89zrl"><a href="/books/NBK83581/table/Fresolimumab89Zr.T.nc_chemical_name89zrl/?report=objectonly" target="object" rid-ob="figobFresolimumab89ZrTncchemicalname89zrl">Table</a></h4><p class="float-caption no_bottom_margin">
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<i>In vitro</i>
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Rodents
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</p></div></div><div id="Fresolimumab89Zr.Background"><h2 id="_Fresolimumab89Zr_Background_">Background</h2><p>[<a href="/pubmed?term=tgf%20beta%20review&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>The transforming growth factor-β (TGF-β) belongs to a superfamily of cytokines that mediate their activity through serine/threonine kinase receptors and are involved in a variety of cellular processes such as proliferation, differentiation, and migration (<a class="bibr" href="#Fresolimumab89Zr.REF.1" rid="Fresolimumab89Zr.REF.1 Fresolimumab89Zr.REF.2">1, 2</a>). The TGF-β is a tumor suppressor, but under certain cellular conditions it can promote tumor progression and cancer metastasis as discussed by Meulmeester and ten Dijke (<a class="bibr" href="#Fresolimumab89Zr.REF.2" rid="Fresolimumab89Zr.REF.2">2</a>) and Inman (<a class="bibr" href="#Fresolimumab89Zr.REF.3" rid="Fresolimumab89Zr.REF.3">3</a>). Although TGF-β and its receptors are considered to be important targets for the treatment of highly invasive tumors such as <a href="http://www.cedars-sinai.edu/Patients/Health-Conditions/Glioblastoma-Multiforme-Brain-Tumors.aspx" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">glioblastomas</a> and those of <a href="http://www.cedars-sinai.edu/Patients/Health-Conditions/Breast-Cancer.aspx" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">breast cancer</a>, no drug or antibody is available to inhibit the activity of this cytokine or its receptor signaling pathway to treat these malignancies (<a class="bibr" href="#Fresolimumab89Zr.REF.4" rid="Fresolimumab89Zr.REF.4">4</a>). A subset of breast cancer patients exhibited overexpression or suppression of genes related to the TGF-β signaling pathway, and these individuals also showed a shorter metastasis-free or relapse-free survival (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). Therefore, noninvasive imaging of TGF-β will not only help in understanding the functioning of this receptor–ligand system and assist in the development of novel agents that can target the TGF-β or its receptor, but it will also assist in the selection of patients who would benefit most from such an anti-cancer treatment (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>).</p><p>Fresolimumab, a human anti-TGF-β monoclonal antibody (mAb) that neutralizes all active isoforms of TGF-β, was developed and used in a phase I study for the treatment of 22 patients with advanced melanoma and renal cell carcinoma (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). After the treatment, one patient showed stable disease, one patient had a partial response, and three patients showed a mixed response. In addition, no dose-limiting toxicity with the Ab was apparent in the patients. To further improve the likelihood of a positive outcome after the treatment with fresolimumab, it would be helpful to know if the TGF-β or its receptor are overexpressed and activated in the tumor, and also whether the mAb is able to detect such tumors. For this, Oude Munnink et al. evaluated <sup>89</sup>Zr-labeled fresolimumab ([<sup>89</sup>Zr]-fresolimumab) for the detection and quantification of tumors that overexpress TGF-β with positron emission tomography (PET) in a nude mouse model (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). The investigators chose to label the mAb with <sup>89</sup>Zr because it has a long half-life (~78 h), and is also suitable to study binding of the labeled antibody to the tumor and to monitor its organ distribution in animal models. The biodistribution of [<sup>89</sup>Zr]-fresolimumab was also studied in mice bearing xenograft tumors that express varying levels of TGF-β.</p><div id="Fresolimumab89Zr.Related_Resource_Links"><h3>Related Resource Links</h3><p><a href="/nuccore/1813326?report=genbank" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">mRNA and Protein</a> sequence of TGF-β (GenBank )</p><p>TGF-β in Online Mendelian Inheritance in Man Database <a href="http://omim.org/entry/190180" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">(OMIM)</a></p><p>TGF-β receptor signaling in <a href="http://pid.nci.nih.gov/search/pathway_landing.shtml?pathway_id=tgfbrpathway&pathway_name=TGF-beta%20receptor%20signaling&source=NCI-Nature%20curated&what=graphic&jpg=on&ppage=1" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Pathway Interaction Database</a></p><p><a href="http://clinicaltrials.gov/ct2/results?term=Transforming+growth+factor" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Clinical trials</a> related to TGF-β</p><p>TGF-β and cancer therapy [<a href="/pubmed?term=TGF%20beta%20and%20cancer%20therapy&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p><a href="http://www.kegg.jp/kegg-bin/search_result?db=disease&lang=&pid=13275085694153&q=TGF%20beta&show=pathway" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">Diseases related to TGF- β</a> (From Kyoto Encyclopedia of Genes and Genomics)</p></div></div><div id="Fresolimumab89Zr.Synthesis"><h2 id="_Fresolimumab89Zr_Synthesis_">Synthesis</h2><p>[<a href="/pubmed?term=89Zr-fresolimumab%20synthesis&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>Fresolimumab was obtained from a commercial source and conjugated with <i>N</i>-succinyldesferrioxamine-B-tetrafluorphenol (<i>N</i>-sucDf-TFP) as detailed by Oude Munnink et al. (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). Fresolimumab and <i>N</i>-sucDf-TFP had an effective conjugation of 62.0 ± 9.0%. <i>N</i>-sucDf-fresolimumab was stored at −20°C until required and was labeled with clinical grade <sup>89</sup>Zr-oxalate on the day of use. The radiochemical purity (RCP) of [<sup>89</sup>Zr]-fresolimumab was 97.0 ± 1.2% as determined with high-performance liquid chromatography (HPLC), and it was used without further purification. The specific activity of the labeled mAb was reported to be up to 1,000 MBq/6.6 nmol (2.7 mCi/6.6 nmol).</p><p>[<sup>89</sup>Zr]-Fresolimumab was stable in 0.9% NaCl at 4°C and in human serum at 37°C for >168 h as determined with HPLC (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>).</p><p>Human IgG was conjugated to 2-(4-isothiocyanatobenzyl)-diethylenetriaminepentaacetic acid and then labeled with <sup>111</sup>In ([<sup>111</sup>In]-IgG) on the required day for use as a control in the biodistribution study (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). The radiochemical yield, RCP, specific activity, and stability of the labeled IgG were not reported.</p></div><div id="Fresolimumab89Zr.In_Vitro_Studies_Testin"><h2 id="_Fresolimumab89Zr_In_Vitro_Studies_Testin_"><i>In Vitro</i> Studies: Testing in Cells and Tissues</h2><p>[<a href="/pubmed?term=89Zr-fresolimumab%20in%20vitro&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>In a competitive TGF-β binding assay with [<sup>89</sup>Zr]-fresolimumab in the presence of increasing concentrations of unlabeled fresolimumab, the 50% inhibition of the maximum binding of labeled fresolimumab was determined to be 14 nM compared with 18 nM for the unlabeled mAb (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). This indicated that conjugating the mAb with <i>N</i>-sucDf-TFP and labeling it with <sup>89</sup>Zr did not alter the affinity of [<sup>89</sup>Zr]-fresolimumab for the ligand.</p></div><div id="Fresolimumab89Zr.Animal_Studies"><h2 id="_Fresolimumab89Zr_Animal_Studies_">Animal Studies</h2><div id="Fresolimumab89Zr.Rodents"><h3>Rodents</h3><p>[<a href="/pubmed?term=89Zr-fresolimumab%20rodentia&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>Two different biodistribution studies were performed with nude mice bearing either Chinese hamster ovary (CHO) cell or human breast cancer MDA-MB-231 cell subcutaneous xenograft tumors as described by Oude Munnink et al. (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>).</p><p>For the CHO cell study, nude mice bore either CHO-Cl11S cell (produces intermediate levels of latent TGF-β; 23.3 ng/10<sup>6</sup> cells/day; determined in the growth medium with ELISA) or CHO-C12 cell (produces high levels of latent TGF-β; 189 ng/10<sup>6</sup> cells/day; determined in the growth medium with ELISA) subcutaneous xenograft tumors. The mice (<i>n</i> = 2–6 animals/dose) were administered [<sup>89</sup>Zr]-fresolimumab (5 MBq (135 μCi) in 66.6 pmol, 333 pmol, or 666 pmol mAb) or [<sup>111</sup>In]-IgG (3 MBq (81 μCi) in 66.6 pmol, 333 pmol, or 666 pmol IgG) through the penile vein. The animals were euthanized at 144 h postinjection (p.i.) to determine the amount of radioactivity accumulated in the various organs of the animals. Data obtained from the study were expressed as percent of injected dose per gram tissue (% ID/g). A comparable uptake of both tracers was observed in all the organs and tumors of the animals, except in the liver and bone, which showed a higher accumulation of label from [<sup>89</sup>Zr]-fresolimumab than from [<sup>111</sup>In]-IgG. Only in the kidneys and liver of mice injected with the 66.6 pmol dose was there a 92 ± 28% (<i>P</i> = 0.0078) and 69 ± 28% (<i>P</i> = 0.0005), respectively, higher uptake of the tracer from [<sup>89</sup>Zr]-fresolimumab than from [<sup>111</sup>In]-IgG. Assessment of TGF-β levels in liver homogenates with ELISA showed there was no increase in the level of the active cytokine in this organ. The investigators suggested that the higher levels of <sup>89</sup>Zr observed in the liver were probably because the breakdown products of [<sup>89</sup>Zr]-fresolimumab had accumulated in the liver or degradation products of TGF-β from other organs that had bound [<sup>89</sup>Zr]-fresolimumab were present in this organ for disposal. A similar trend was observed in the tumors of mice bearing the CHO-C12 or CHO-Cl11S xenografts.</p><p>Small-animal PET images were acquired from mice bearing the CHO-Cl11S or CHO-C12 cell xenograft tumors at 24, 72, and 144 h p.i (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). No difference in the uptake of radioactivity from [<sup>89</sup>Zr]-fresolimumab was apparent from the PET images of the tumors from the two CHO clones. No single-photon emission computed tomography images of animals injected with [<sup>111</sup>In]-IgG were reported for comparison with the images obtained with [<sup>89</sup>Zr]-fresolimumab. In addition, hematoxylin and eosine staining showed no morphological differences between the xenograft tumors originating from either CHO clone.</p><p>In another study, the MDA-MB-231 cell human breast cancer xenograft mouse model (number of mice used for the study was not reported) was used to study the biodistribution of [<sup>89</sup>Zr]-fresolimumab (5 MBq (135 μCi) in 66.6 pmol/animal) and [<sup>111</sup>In]-IgG (3 MBq (81 μCi) in 66.6 pmol/animal) (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). The biodistribution of label from both radiolabeled immunoreagents was similar to that observed during the CHO studies mentioned above.</p><p>Because breast cancer is often metastasized to the bone, [<sup>89</sup>Zr]-fresolimumab was also evaluated for the visualization of bone metastasis in a mouse metastatic breast cancer model (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>). The animals developed bone metastasis 3–5 weeks after intracardiac injection of MDA-MB-231-SCP2luc cells (a bone tropic clone of MDA-MB-231 cells that are transfected with a luciferase and described elsewhere (<a class="bibr" href="#Fresolimumab89Zr.REF.6" rid="Fresolimumab89Zr.REF.6">6</a>)). The metastasis was confirmed in the animals with bioluminescence imaging (BLI) and was located mainly in the jaws, skull, sternum, spine shoulders, hips, and lower limbs of the animals. The mice were injected with [<sup>89</sup>Zr]-fresolimumab, and small-animal PET images were acquired as before. The investigators reported that neither micro-computed tomography nor small-animal PET could detect the metastasis visualized with BLI.</p><p>From these studies, the investigators concluded that [<sup>89</sup>Zr]-fresolimumab can be used with small-animal PET to visualize neoplastic tumors that express TGF-β in mice (<a class="bibr" href="#Fresolimumab89Zr.REF.5" rid="Fresolimumab89Zr.REF.5">5</a>).</p></div><div id="Fresolimumab89Zr.Other_NonPrimate_Mammal"><h3>Other Non-Primate Mammals</h3><p>[<a href="/pubmed?term=89Zr-fresolimumab%20Non-Primate%20Mammals&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p></div><div id="Fresolimumab89Zr.NonHuman_Primates"><h3>Non-Human Primates</h3><p>[<a href="/pubmed?term=89Zr-fresolimumab%20Non-Human%20Primates&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p></div></div><div id="Fresolimumab89Zr.Human_Studies"><h2 id="_Fresolimumab89Zr_Human_Studies_">Human Studies</h2><p>[<a href="/pubmed?term=89Zr-fresolimumab%20Human%20Studies&cmd=DetailsSearch" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubMed</a>]</p><p>No publication is currently available.</p></div><div id="Fresolimumab89Zr.Supplemental_Informatio"><h2 id="_Fresolimumab89Zr_Supplemental_Informatio_">Supplemental Information</h2><p>[<a href="/books/n/micad/disclaimer/?report=reader">Disclaimers</a>]</p><p>No information is currently available.</p></div><div id="Fresolimumab89Zr.References"><h2 id="_Fresolimumab89Zr_References_">References</h2><dl class="temp-labeled-list"><dl class="bkr_refwrap"><dt>1.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.1">Hawinkels L.J., Ten Dijke P.
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<em>Exploring anti-TGF-beta therapies in cancer and fibrosis.</em>
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<span><span class="ref-journal">Growth Factors. </span>2011;<span class="ref-vol">29</span>(4):140–52.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/21718111" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21718111</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>2.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.2">Meulmeester E., Ten Dijke P.
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<em>The dynamic roles of TGF-beta in cancer.</em>
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<span><span class="ref-journal">J Pathol. </span>2011;<span class="ref-vol">223</span>(2):205–18.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/20957627" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 20957627</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>3.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.3">Inman G.J.
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<em>Switching TGFbeta from a tumor suppressor to a tumor promoter.</em>
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<span><span class="ref-journal">Curr Opin Genet Dev. </span>2011;<span class="ref-vol">21</span>(1):93–9.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/21251810" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21251810</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>4.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.4">Garber K.
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<em>Companies waver in efforts to target transforming growth factor beta in cancer.</em>
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<span><span class="ref-journal">J Natl Cancer Inst. </span>2009;<span class="ref-vol">101</span>(24):1664–7.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/19933941" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 19933941</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>5.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.5">Oude Munnink T.H., Arjaans M.E., Timmer-Bosscha H., Schroder C.P., Hesselink J.W., Vedelaar S.R., Walenkamp A.M., Reiss M., Gregory R.C., Lub-de Hooge M.N., de Vries E.G.
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<em>PET with the 89Zr-Labeled Transforming Growth Factor-beta Antibody Fresolimumab in Tumor Models.</em>
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<span><span class="ref-journal">J Nucl Med. </span>2011;<span class="ref-vol">52</span>(12):2001–8.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/22072706" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 22072706</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>6.</dt><dd><div class="bk_ref" id="Fresolimumab89Zr.REF.6">Minn A.J., Kang Y., Serganova I., Gupta G.P., Giri D.D., Doubrovin M., Ponomarev V., Gerald W.L., Blasberg R., Massague J.
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<em>Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors.</em>
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<span><span class="ref-journal">J Clin Invest. </span>2005;<span class="ref-vol">115</span>(1):44–55.</span> [<a href="/pmc/articles/PMC539194/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC539194</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/15630443" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15630443</span></a>]</div></dd></dl></dl></div><div id="bk_toc_contnr"></div></div></div><div class="fm-sec"><h2 id="_NBK83581_pubdet_">Publication Details</h2><h3>Author Information and Affiliations</h3><div class="contrib half_rhythm"><span itemprop="author">Arvind Chopra</span>, PhD<div class="affiliation small">National Center for Biotechnology Information, NLM, Bethesda, MD 20894<div><span class="email-label">Email: </span><a href="mailto:dev@null" data-email="vog.hin.mln.ibcn@dacim" class="oemail">vog.hin.mln.ibcn@dacim</a></div></div></div><h3>Publication History</h3><p class="small">Created: <span itemprop="datePublished">December 13, 2011</span>; Last Update: <span itemprop="dateModified">January 26, 2012</span>.</p><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="http://www.ncbi.nlm.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Center for Biotechnology Information (US)</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>Chopra A. 89Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody) 2011 Dec 13 [Updated 2012 Jan 26]. In: Molecular Imaging and Contrast Agent Database (MICAD) [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2004-2013. <span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"><a href="/books/n/micad/Onartuzumab-Df-89Zr/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M75,30 c-80,60 -80,0 0,60 c-30,-60 -30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Prev</text></svg></a></div><div class="small-screen-next"><a href="/books/n/micad/Rzumab89Zr/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M25,30c80,60 80,0 0,60 c30,-60 30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Next</text></svg></a></div></article><article data-type="table-wrap" id="figobFresolimumab89ZrTncchemicalname89zrl"><div id="Fresolimumab89Zr.T.nc_chemical_name89zrl" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK83581/table/Fresolimumab89Zr.T.nc_chemical_name89zrl/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__Fresolimumab89Zr.T.nc_chemical_name89zrl_lrgtbl__"><table><tbody><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Chemical name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;"><sup>89</sup>Zr-Labeled fresolimumab (human anti-transforming growth factor-β monoclonal antibody)</td><td rowspan="9" colspan="1" style="text-align:center;vertical-align:middle;"></td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Abbreviated name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">[<sup>89</sup>Zr]-Fresolimumab<br /></td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Synonym:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">GC1008 (produced by Genzyme)</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Agent Category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Antibody</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Transforming growth factor-β</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target Category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Antigen</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Method of detection:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Positron emission tomography (PET)</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Source of signal / contrast:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;"><sup>89</sup>Zr</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Activation:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">No</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Studies:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">
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<ul class="simple-list"><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" />
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<i>In vitro</i>
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</div></li><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" /> Rodents
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</div></li></ul>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Structure not available in <a href="http://pubchem.ncbi.nlm.nih.gov/" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">PubChem</a>.</td></tr></tbody></table></div></div></article></div><div id="jr-scripts"><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/libs.min.js"> </script><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.min.js"> </script></div></div>
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