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Novel applications for Ex-vivo PDX models of the Tumor Microenvironment

Ex-vivo platforms are useful to gain data regarding the efficacy of an oncology treatment throughout the course and after completion of a study. Furthermore, ex-vivo assays can be used to unravel mechanisms of action for immuno-oncology agents and assess cytotoxicity of oncology therapeutics. In this webinar, case studies will be discussed to demonstrate physiologically relevant 2D and 3D ex vivo PDX Models for testing oncologic therapeutic agents.

Register for this webinar to learn:
• How to combine physiologically relevant 2D and 3D ex vivo PDX models with quantitative fluorescence imaging and luminescence assays to determine efficacy of oncology treatments.
• The advantages of using tumor fragments vs. other 3D systems.
• How incorporating a diversity of readouts, including industry standard CellTiter Glow and fluorescence microscopy, can provide comprehensive insights to drive oncology research programs forward.
• How adapting different experimental parameters, i.e. drug combinations and treatment length (3 days to 21-day assays), as well as the readouts (RNA/Protein isolation) can improve richness of data we can obtain from a study.
Recorded Sep 24 2020 38 mins
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Presented by
Veronica Sacchi, PhD, Scientist III, PhenoVista Biosciences
Presentation preview: Novel applications for Ex-vivo PDX models of the Tumor Microenvironment

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  • Approaches & Challenges in Choosing the Right Translational Oncology Indication Oct 27 2021 9:00 am UTC 90 mins
    Zaki Sellam, Gary Brandam, Emmanuel Grillot, Alex Moreau
    In this innovative panel discussion, industry leaders will gather to share strategies and tactics on how to choose a translational oncology indication in research & development, what data drives that choice, and determine how any potential pitfalls can be avoided.

    Key discussion topics tackled in this panel discussion:
    - When and how to choose an indication?
    - Can it be purely data-driven?
    - How translational/experimental studies, especially with PDX models could drive such a choice?
    - What about OMICS data? How can it help?
    - What are the pitfalls to be avoided?
    - What about clinical feasibility? How shall it be considered?
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    - Discovery of a potent and selective GPR65 antagonist for “macrophage conditioning” in IO
    - Assessment of the effects of an orally administered GPR65 antagonist in a PDX model of clear cell renal carcinoma
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  • How to Make Preclinical Research a SUCCESS Recorded: Jan 27 2021 90 mins
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    Join the revolution in drug development, based upon forward thinking study design and experimental approaches that are predictive of drug candidates delivering real patient benefit.
    In these difficult times we all must find ways to do more with less. It is more critical than ever to improve the efficiency of the preclinical portfolio and make the most of the limited R&D budget, which allows us all to look into reforming how we look at preclinical research and what we consider ‘success’.
    Our four highly experienced experts, will walk you through what they learned through their own mistakes and are going to share their advice on how to stay competitive in today’s research landscape. You’ll hear how to:
    •Put together an appealing package of new ideas to present to decision makers/venture capitalists/investors
    •How to establish a successful relationship with VCs and CROs: avoid the common mistake and ill-informed decisions in the early stages of the development pipeline
    •Be translational from the get-go to reduce the fail rate of drugs in clinical phase.
    •Work with Contract Research Organisations and leverage the expertise of Translational Oncology experts to run SUCCESSful preclinical studies.
  • Development of a 3D organoid autologous TIL co-culture platform for IO studies Recorded: Dec 1 2020 23 mins
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    Champions Oncology was excited to participate in the Society for Immunotherapy of Cancer’s (SITC) Virtual Meeting in November. Due to the limited availability of access to these posters, we wanted to give you direct access to our expert researchers and all the details of the newest innovations happening at Champions. Therefore, we have set up a Poster Talk with an expert presenter so that you can register, attend and ask questions live during the session – just like you were at SITC2020 face-to-face.

    The preclinical screening of immune-modulatory therapies suffers from the absence of models that recapitulate in vivo heterogeneous tumor microenvironment (TME). 3D tumor organoid cultures provide a model that closely mimics in situ tumor architecture and is being aggressively used to evaluate therapeutic efficacy ex vivo. A vastly heterogenous TME impacts patient treatment response, and there is a dearth of human tumor models (2D or 3D), that mimic in vivo diversity of TME, including infiltrating immune populations. 3D organoid cultures typically contain neoplastic epithelium; however they fall short in representing tumor to tumor-infiltrating lymphocytes (TILs) interactions, limiting their ability to generate clinically relevant response to immunotherapeutics. Addition of immune cells from unrelated donors to organoids can simulate that microenvironment but is complicated by T cell alloreactivity. Here we describe 3D patient-derived xenograft organoid (PDXO) co-cultures with matching autologous human TILs to recapitulate the tumorspecific immune response, leveraging confocal high content analysis and Luminex multiplex assays. This platform allows the evaluation and high throughput screening of novel immune targeting agents to determine impacts on patient-derived T cell function, T cell infiltration, and tumor cytotoxicity.
  • LUMIN: Harnessing the Power of Pharmaco-omics to Illuminate Tumor Cell Biology Recorded: Sep 24 2020 48 mins
    Michael Ritchie, PhD, MBA, Champions Oncology, Chief Commercial Officer
    Data drives every great discovery in modern-day science. At Champions Oncology, we deliver innovative solutions to accelerate oncology drug development. Lumin is that innovative solution. Lumin is a revolutionary data interpretation software capable of analyzing proteomic, genomic and transcriptomic datasets in real time, giving scientists novel insights at their fingertips. The power of Lumin is in the ability to explore data assembled from over 13,000 cancer patients, including thousands of clinical treatment responses not available in any public dataset. In this webinar, case studies will be presented to demonstrate the many different ways to use our newest bioinformatics solution, Lumin.

    Register for this webinar to learn more about Lumin and:
    •Analyze pharmaco-omic relationships across 13,000+ datasets, including Champions’ PDX compendium of 1000 tumor models with known clinical responses.
    •Use external processed pharmaco-omic data for a personalized experience.
    •Investigate gene signatures and biomarker pathways to discover new hypotheses.
  • Novel applications for Ex-vivo PDX models of the Tumor Microenvironment Recorded: Sep 24 2020 38 mins
    Veronica Sacchi, PhD, Scientist III, PhenoVista Biosciences
    Ex-vivo platforms are useful to gain data regarding the efficacy of an oncology treatment throughout the course and after completion of a study. Furthermore, ex-vivo assays can be used to unravel mechanisms of action for immuno-oncology agents and assess cytotoxicity of oncology therapeutics. In this webinar, case studies will be discussed to demonstrate physiologically relevant 2D and 3D ex vivo PDX Models for testing oncologic therapeutic agents.

    Register for this webinar to learn:
    • How to combine physiologically relevant 2D and 3D ex vivo PDX models with quantitative fluorescence imaging and luminescence assays to determine efficacy of oncology treatments.
    • The advantages of using tumor fragments vs. other 3D systems.
    • How incorporating a diversity of readouts, including industry standard CellTiter Glow and fluorescence microscopy, can provide comprehensive insights to drive oncology research programs forward.
    • How adapting different experimental parameters, i.e. drug combinations and treatment length (3 days to 21-day assays), as well as the readouts (RNA/Protein isolation) can improve richness of data we can obtain from a study.
  • Embracing variation: a multi-batch study delivers robust estimates of efficacy Recorded: Sep 24 2020 36 mins
    Natasha A Karp, PhD, Principal Biostatistician in Discovery Sciences, AstraZeneca
    Phenotypic plasticity, the ability of a living organism to respond to the environment, can lead to conclusions from experiments that are idiosyncratic to a particular environment. The level of environmental responsiveness can result in difficulties in reproducing studies from the same institute with the same standardised environment. Here we present a multi-batch approach to in-vivo studies to improve replicability of the results for a defined environment. These multi-batch experiments consist of small independent mini-experiments where the data are combined in an integrated data analysis to appropriately assess the treatment effect after accounting for the structure in the data. We demonstrate the method on two case studies with syngeneic tumour models which are challenging due to high variability both within and between studies. Through simulations and discussions, we explore the optimum design that balances practical constraints of working with animals versus sensitivity and replicability. Through the increased confidence from the multi-batch design, we reduce the need to replicate the experiment, which can reduce the total number of animals used.

    3 take home messages:
    • The historic definition of Reduction, focused on absolute number of animals within a single highly standardised experiment, is not fit for purpose as it leads to experiments with highly context dependent conclusions which are not robust.

    • A multi-batch design embraces the concept of replication and through integrated data analysis allows a reduction in animal usage by planning to integrate studies from the offset.

    • Immuno-oncology tumour studies provide a compelling example of the confidence obtained from exploring a treatment effect across three separate experiments where findings were seen with independent batches of animals, cell cultures etc.
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    Parthanatos (a programmed necrosis from PARP1 hyperactivation) is an untapped death mechanism in oncology, and it offers some ideal features for cancer treatments including immunogenicity and its independence from the drug resistance-ridden p53-apoptosis pathway. Xylonix has developed several synthetic peptide-conjugate APIs including C005D-Zn, C008D-Zn, and C010DS-Zn that were designed to induce parthanatos in cancer, and to varying degrees, M2-like macrophages (M2) with increasing cytotoxicity to both targets in higher-numbered agents. Previously known as the pro-tumor immunity that hampered cancer immunotherapy advances, M2 was also discovered to play the central role in generating both the acute severe cytokine storm and long-term thrombotic complications of COVID19. In the context of the pandemic Xylonix is now focusing to fast-track the C010DS-Zn development with its first target in-human trials against COVID19 with subsequent expansions into oncology and other M2-driven autoimmune diseases. In this talk, I share Xylonix strategy and some breakthrough data for supporting such development goals via aggressive utilization of mechanism studies, genomic information, and large-scale screenings.
  • High-Definition Spatial Proteomics for Characterizing the Tumor Microenvironment Recorded: Sep 23 2020 35 mins
    Jason Ptacek, PhD, Associate Director of Research Services, IONpath, Inc.
    The complexity of the TME with variable cellular composition and organization has driven the development of experimental techniques capable of tracking large numbers of biomarkers in tissue with sub-cellular resolution. This webinar will provide an overview of how high-definition spatial proteomics, enabled by Multiplexed Ion Beam Imaging (MIBI), can be used to explore the tumor microenvironment (TME) of tumor biopsy samples with unprecedented depth. MIBI leverages the high resolution of a rastered primaryion beam and the sensitivity of time-of-flight secondary ion mass spectrometry (ToF-SIMS) to image standard frozen or formalin fixed paraffin embedded (FFPE) tissue sections that have been stained with up to 40 different antibodies labeled with metal isotope tags. Masses of detected species are assigned to target biomolecules given the unique label of each antibody. Multi-step processing and segmentation utilizing highly expressed nuclear, membrane, and cytoplasmic markers are then performed to accurately determine cell boundaries. Cell classification is performed to phenotypically characterize the tissue environments and quantify marker expression. Dr. Jason Ptacek, Associate Director of Research Services at IONpath, Inc., will share examples of quantitative single-cell phenotype mapping in tissue analysis applications and review the data analysis methods used to generate actionable insights from this highly multiplexed, spatial proteomic data.

    Learn how MIBI provides:
    ● Comprehensive, quantitative single-cell phenotyping across tumor samples
    ● Characterization of the spatial organization of cell populations of the TME
    ● Sensitivity to quantify the expression of markers associated with immune suppression
  • Selective Ablation of Malignant Cells using Apoptotic Gene Therapy Recorded: Sep 23 2020 34 mins
    Jailal Ablack, PhD, Head of Preclinical Research, OncoSenX
    While chemotherapy is a key treatment strategy for many solid tumors, it is rarely selective for tumor cells. OncoSenx has developed an effective suicide gene therapy approach to eliminate solid tumors based on their unique sate of transcriptional activation. The p53 tumor suppressor is frequently mutated or dysregulated in cancers and as a result the upstream signaling pathways activating TP53 transcription are strongly upregulated. We exploit this under appreciated feature of the p53 tumor suppressor pathway to target malignant cells. Leveraging the Fusogenix Proteo-Lipid Vehicle platform, a p53-driven inducible suicide gene, iCasp9, is delivered systemically. In malignant cells where the p53 pathway is upregulated the inducible suicide gene is expressed and upon activation with a chemical activator tumor cells rapidly undergo apoptosis eliminating solid tumors. As a single agent our suicide gene therapy out performs checkpoint blockade as a single agent and synergizes in combination with checkpoint blockade to produces curative and durable control of CT26 tumors.

    Key Take Aways:
    • Mutation/ablation of the p53 Tumor suppressor results in upregulation the TP53 locus.
    • An engineeredTP53 promoter can selectively kill malignant cells in vitro and in vivo.
    • This approach synergizes with checkpoint blockade.
  • Evaluation of Acute Myeloid Leukemia by high parameter flow cytometry Recorded: Sep 23 2020 28 mins
    Greg Bannish, PhD, Flow Cytometry Subject Matter Expert, Champions Oncology
    Acute Myeloid leukemia (AML) is a specific type of cancer in which the bone marrow makes abnormal myeloblasts, red blood cells and platelets. AML is the most prevalent acute leukemia in adults. Champions Oncology has developed and optimized an 18-color Comprehensive AML Flow Cytometry panel for use in preclinical primary AML models and for exploratory clinical studies. This webinar will walk through the development of the panel and its uses from the bench to the clinic.

    Learning points for this webinar:
    • Use of flow cytometry in detection of AML
    • Delineation of phenotype markers in different AML subtypes
    • Detection of rare cell subsets and correlation with drug treatment
  • Targeting IDH mutations in Cancer Recorded: Sep 23 2020 34 mins
    Brandon Nicolay, PhD, Associate Director, Pharmacology, Agios Pharmaceuticals
    Somatic mutations in the enzyme isocitrate dehydrogenase 1 (IDH1) arise in roughly 6–10% of patients with acute myeloid leukemia (AML). These mutations interfere with epigenetic control of gene expression, which prevents hematopoietic cell maturation. Ivosidenib (IVO; AG-120) is an oral, potent, targeted inhibitor of mutant IDH1(mIDH1)and is FDA-approved for the treatment of patients with mIDH1relapsed/refractory, patients with mIDH1 newly diagnosed AML who are ≥ 75 years of age or have comorbidities that preclude intensive induction chemotherapy. Currently, IVO is being investigated in combination with azacytidine (AZA) in adult participants with previously untreated mIDH1AMLin the actively enrolling phase 3 AGILE study (NCT03173248). To support this ongoing effort, studies were undertaken to explore the IVO+ AZA combination in a mIDH1AML patient-derived xenograft (PDX)model in vivo.

    Additionally, ongoing preclinical studies have been underway to examine the timing of IVO+ AZA treatment with respect to disease burden control and durability in mice inoculated with a disseminated mIDH1AML PDX model; both as an up-front treatment as well as in a maintenance therapy setting following either venetoclax (VEN) + AZA, or VEN + AZA + IVO. Initial findings from these murine AML PDX studies support the reported clinical observation that IVO + AZA combination treatment is superior at controlling mIDH1AML disease burden compared with either agent alone. Together, these data will enhance our understanding of how to best combine the use of these agents to achieve long term disease control.

    3 Key Takeaways:
    • Ivosidenib is an FDA-approved targeted inhibitor of mIDH1that acts to promote hematopoietic cell maturation in AML
    • Murine studies indicate that IVO+ AZA combination treatment is superior at controlling mIDH1AML disease burden compared withIVO or AZA alone
    • IVO+ AZA is being investigated in participants with untreated mIDH1AMLin the phase 3 AGILE study
  • Human-derived IO preclinical systems—from in vitro to in vivo and back Recorded: Sep 23 2020 39 mins
    Amy Wesa, PhD, Head of R&D, Champions Oncology
    Immuno-oncology (IO) is the study and development of treatments that take advantage of the body’s immune system to fight cancer. IO research has been growing over the years with the addition of new immunotherapies and development of biologic drugs that target the inhibition of immune checkpoints and other mechanisms of action. In this webinar, Dr. Wesa will demonstrate how human-derived immune-oncology preclinical systems can be used to advance drug development.

    Viewing this webinar will help you to:
    • Compare strengths and limitations of in vivo humanized platforms
    • Assessing the appropriate system for distinct I-O therapeutic targets
    • Go back to basics: ex vivo patient-derived tumor co-culture models
  • Tipifarnib as a Precision Therapy for HRAS-Mutant Head and Neck SCCs Recorded: Sep 22 2020 43 mins
    Francis Burrows, PhD, VP of Translational Research, Kura Oncology
    Tipifarnib is a potent and highly selective inhibitor of farnesyltransferase (FT). FT catalyzes the post-translational attachment of farnesyl groups to signaling proteins that are requiredfor localization to cell membranes. Althoughall RAS isoforms are FT substrates, only HRAS is exclusively dependent upon farnesylation, raising the possibility that HRAS mutant tumors might be susceptible to tipifarnib-mediated inhibition of FT. Here,we report the characterization of tipifarnib activity in awidepanel of HRASmutant and wild type HNSCC xenograft models. Tipifarnib treatment displaced both mutant and wild type HRAS from membranes but only inhibited proliferation, survival and spheroid formation of HRASmutant cells. In vivo, tipifarnib treatment induced tumor stasis or regression in all six HRASmutant xenografts tested but displayed no activity in six HRASwild type PDX models. Mechanistically, drug treatment resulted in reduction of MAPK pathway signaling, inhibition of proliferation and induction of apoptosis and robust abrogation of neovascularization, apparently viaeffects on both tumor cells and endothelial cells. Bioinformatics and quantitative image analysis further revealed that FT inhibition induces progressive squamous cell differentiation in tipifarnib-treated HNSCC PDX. These preclinical findings support that HRASrepresents a druggableoncogenein HNSCC through FT inhibition by tipifarnib, thereby identifying a precision therapeutic option for HNSCCs harboring HRASmutations.
  • Models for evaluating cancerous stem cell-targeting therapeutics Recorded: Sep 22 2020 34 mins
    Lynn Biderman, PhD, Senior Scientist, Stelexis Therapeutics
    Cancer formation and progression are largely driven by cancerous stem cells (CSCs). CSCs are typically not eliminated by conventional treatment approaches, creating an unmet need for developing innovative therapeutics to prevent disease recurrence and relapse. While CSCs are rare in patient specimens, Stelexis Therapeutics, through its proprietary Tumor OriginTM Platform, can isolate and expand this rare CSC population from a wide collection of patient-derived samples, while maintaining their clinical relevance. Utilizing the Tumor OriginTM Platform, we were able to discover novel, druggable CSC targets and to develop high affinity neutralizing monoclonal antibodies (mAbs). Patient-derived models have been instrumental in evaluating our therapeutic mAbs in both AML and solid tumors. In AML, an in vitro drug sensitivity screen guided our selection of models for in vivo PDX studies. Immuno-deficient mice were injected with patient-derived AML cells, monitored for engraftment, and treated with our mAbsas mono therapy or in combination with standard of care. Study readout comprised of monitoring disease burden, as indicated by the count of different human hematopoietic cells in the blood, the bone marrow and the spleen. To study the effect of our therapeutic antibodies on solid tumors, we employed two models: PDX models engrafted in the flank, followed by tumor volume monitoring, and lung inflammation and metastasis assessment, and cancer cells injected into the tail vein and assessed for lung seeding, metastasis formation and tissue inflammation.

    Key points:
    •There is a great unmet need in targeting CSCs for treating cancer progression and relapse
    •Stelexis Therapeutics has developed the Tumor OriginTM Platform for the isolation, expansion and maintenance of patient-derived CSCs that enables novel target & drug discovery
    •Patient-derived models have supported our pre-clinical proof of concept studies in AML & solid tumors, both in vitro & in mouse xenograft models
  • Constrained bicyclic peptide delivery of toxin & immune agonists to solid tumors Recorded: Sep 22 2020 32 mins
    Johanna Lahdenranta, PhD, Director, In Vivo Pharmacology, Bicycle Therapeutics
    We have developed tumor-targeted toxin conjugates (Bicycle toxin conjugates, BTCs) as well as tumor targeted immune cell agonists (TICAs™) based on constrained bicyclic peptides (Bicycles®) by linking toxins such as MMAE or Bicycles against costimulatory receptors (e.g. CD137) to those against tumor antigens (e.g. EphA2 or Nectin-4). EphA2-targeted Bicycle toxin conjugate BT5528 gives rise to rapid update into tumors and fast renal elimination followed by persistent toxin levels in tumors without prolonged exposure of parent drug in the vasculature. This fast in, fast out kinetics gave rise to more favorable toxicology findings in rats and monkeys than were observed with MEDI-547 in preclinical and clinical studies. BT5528 dosing is underway in Phase I/II study in patients with advanced solid tumors. Nectin-4 targeted CD137 TICA is a potent agonist that activates costimulatory receptors selectively in the presence of tumor cells. Treatment of tumor antigen -expressing tumors in immunocompetent mice with TICAs lead to profound reprogramming of the tumor immune microenvironment including increased T cell infiltration and increase in cytotoxic cell gene signature. This leads to cytotoxic T cell -dependent complete tumor regressions and resistance to tumor re-challenge. Despite fairly short plasma half-lives in mice (1 – 2h), intermittent dosing of TICAs is very effective indicating potential for a wide therapeutic index in humans. Cell line and patient derived tumor xenograft models as well as transgenic huCD137 syngeneic mouse tumor models have been instrumental in the preclinical development of BTCs and TICAs.
  • Targeting Notch Altered Patient Derived Xenografts (PDX) with AL101 Recorded: Sep 22 2020 28 mins
    Joel Kaye, PhD, VP Research & Nonclinical Development, Ayala Pharmaceuticals
    Notch pathway activation has been implicated in the development of cancer. Notch cleavage by γ-secretase frees the Notch intracellular domain (NICD), which promotes the expression of target genes involved in tumorigenesis. Tumors in which Notch has an oncogenic role often harbor activating alterations that promote ligand-independent Notch cleavage generating high levels of NICD, or alternatively alterations that result in sustained activity of NICD. Notch activating alterations have been found in several cancers including Adenoid Cystic Carcinoma (ACC) and Triple Negative Breast Cancer (TNBC).AL101 is an investigational small molecule pan-Notch γ-secretase inhibitor, previously testedin 3 Phase I trials as monotherapy or in combination regimens in > 200 solid/hematologic cancer patients. Here, we describe the preclinical work evaluating the effect of AL101 patient derived xenograft (PDX) tumor models with Notch activating genetic alterations.

    We demonstrate that PDX tumors bearing Notch activating genetic alterations are exquisitely sensitive to AL101 monotherapy. In both ACC & TNBC models, significant tumor growth inhibition (TGI) was seen only in Notch activated models. AL101 had nosignificant effect on tumors lacking Notch activating mutations. In addition, we also analyzed the effect of AL101 on Notch target genes using RNA-Seq and Western blot or Immunohistochemistry (IHC).

    These data support the clinical development of AL101 asa targeted therapy for tumors bearing Notch activating genetic alterations. Indeed, we are currently investigating AL101 in 2 Phase II open-label, single-arm, multicenter study in ACC patients (ACCURACY; NCT03691207) or TNBC (TENACITY; NCT04461600) harboring known Notch1-4 activating alterations
  • Cell cycle intervention beyond Palbociclib; discovery of a CDK2/4/6 inhibitor Recorded: Sep 22 2020 51 mins
    Stephen Dann, PhD, Associate Research Fellow, Pfizer
    Phosphorylation of the retinoblastoma protein (RB1) by cyclin-dependent kinases (CDK) 4 and 6 is a critical checkpoint for G1/S cell cycle progression and commitment to cellular proliferation. Palbociclib(IBRANCE®), a highly selective inhibitor of CDK4/6, significantly improves progression free survival, and is approved for prescription use, in hormone receptor positive (HR+) HER2 negative breast cancer when combined with an anti-hormonal agent. In anticipation of intrinsic and acquired therapy-refractory disease we sought to discover CDK4/6 inhibitor resistance mechanisms in preclinical models of cancer which coalesced on the induction of Myc oncogene and Cylin E/CDK2 activity. We propose that targeting the G1kinases CDK2, -4 and -6 with a single small molecule inhibitor will overcome CDK4/6 inhibitor resistance. CDK1 and CDK9 anti-targets share several physical structure characteristics with the G1kinases making chemical design iterations particularly challenging. Relying heavily on advanced structure-based drug design techniques, PF-06873600, a pyridopyrimidine with potent biochemical activity on CDK2/4/6 and >40 fold selectivity over anti-targets, was characterized in models of CDK2 and CDK4/6 driven tumor growth for pharmacodynamic and efficacy response. Further, Myc driven molecular correlates of response were identified for PF-06873600 across multiple tumor lineages. Finally, we find that even under drug pressure, where the G1 CDKs are inhibited, the tumor specific immune response that occurs during checkpoint blockade remains intact in syngeneic models of cancer. We anticipate that PF-06873600 will offer a novel therapeutic option to cancer patients where CDK4/6 inhibition is not or is no longer beneficial to blocking disease progression.
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  • Title: Novel applications for Ex-vivo PDX models of the Tumor Microenvironment
  • Live at: Sep 24 2020 5:30 pm
  • Presented by: Veronica Sacchi, PhD, Scientist III, PhenoVista Biosciences
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