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Abbreviations:

4-1BB, tumor necrosis factor receptor superfamily member 9; ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia; APRIL, a proliferation inducing ligand; BAFF, B-cell activating factor from the tumor necrosis factor family; BAK, Bcl-2 homologous antagonist killer; BAX, Bcl-2-associated X protein; BCL-2, B-cell lymphoma 2; BCMA, B-cell maturation antigen; BCR, B-cell receptor; BH, Bcl-2 homology domain; BiTE, Bispecific T-cell Engager; C5, complement component 5; CD, cluster of differentiation; CIT, chemotherapy-induced thrombocytopenia; CLDN18.2, Claudin-18 isoform 2; DARPin, designed ankyrin repeat proteins; DLBCL, diffuse large B-cell lymphoma; DLL3, delta-like protein 3; EGFR, epidermal growth factor receptor; EGFRvIII, epidermal growth factor receptor variant III; Fab, fragment antigen-binding; FAP, fibroblast activation protein; Fc, fragment crystallizable; FLT3, fms-like tyrosine kinase 3; GEJ, gastroesophageal junction; GM-CSF, granulocyte-macrophage colony-stimulating factor; GvHD, graft versus host disease; HCC, hepatocellular carcinoma; HLE, half-life extended; IL-2R, interleukin 2 receptor; IL-21R, interleukin 21 receptor; IL-2Rα, interleukin 2 receptor alpha; KRAS, Kirsten rat sarcoma; MAC, membrane attack complex; MCL-1, myeloid cell leukemia-1; mCRPC, metastatic castration-resistant prostate cancer; MetMel, metastatic melanoma; MM, multiple myeloma; MOA, mechanism of action; MUC17, mucin 17; NHL, non-Hodgkin's lymphoma; NSCLC, non-small cell lung cancer; PD-1, programmed cell death protein 1; PD-L1, programmed cell death ligand 1; PD-L2, programmed cell death ligand 2; PNH, paroxysmal nocturnal hemoglobinuria; PSA, prostate-specific antigen; PSMA, prostate-specific membrane antigen; RAS, rat sarcoma; R/R, relapsed or refractory; SCLC, small cell lung cancer; STEAP1, six-transmembrane epithelial antigen of prostate 1; TPO, thrombopoietin; TPO-R, thrombopoietin receptor; Treg, regulatory T cell.

Amgen Oncology
Pipeline

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SOLID MALIGNANCIES

MALIGNANCIES

TARGETS

HEMATOLOGIC DISEASES

DISEASES

TARGETS

PIPELINE

BITE® PLATFORM

BIOSIMILARS

MODALITIES

ONCOLYTICS

Physicians have long observed that certain viruses can slow the progression of cancer. Oncolytic immunotherapy aims to harness this potential by using genetically modified viruses to target tumors in several important and complementary ways.1

By deleting certain genes, viruses can be reprogrammed to replicate in tumor cells but not in normal cells.1,2 This selective viral replication causes the tumor cells to lyse—releasing tumor-specific antigens.1 The virus can also be modified to produce human GM-CSF, signaling dendritic cells to the site of the lysed tumors where they encounter tumor antigens—generating a broad immunotherapeutic response that can help cytotoxic T cells to recognize and attack distant metastases throughout the body.2,3

GM-CSF, granulocyte-macrophage colony-stimulating factor; HCC, hepatocellular carcinoma; MetMel, metastatic melanoma; MOA, mechanism of action.

References
1. Choi AH, et al. Biomedicines. 2016;4:18. doi:10.3390/biomedicines4030018. 2. Andtbacka RHI, et al. J Clin Oncol. 2015;33:2780-2788. 3. Chen DS, et al. Immunity. 2013;39:1-10. 4. Amgen Pipeline. https://www.amgenpipeline.com. Accessed 9/10/20. 5. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02263508. Accessed 9/10/20. 6. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT04068181. Accessed 9/4/20. 7. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02910557. Accessed 9/10/20. 8. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02509507. Accessed 9/10/20. 9. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02756845. Accessed 9/10/20. 10. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT03256344. Accessed 9/10/20.
Molecule
Modality4
Target1,4
Areas of Investigation5-10
Talimogene laherparepvec
Modality4
ONCOLYTICS
Target1,4
Areas of Investigation5-10

GM-CSF, granulocyte-macrophage colony-stimulating factor; HCC, hepatocellular carcinoma; MetMel, metastatic melanoma; MOA, mechanism of action.

References
1. Choi AH, et al. Biomedicines. 2016;4:18. doi:10.3390/biomedicines4030018. 2. Andtbacka RHI, et al. J Clin Oncol. 2015;33:2780-2788. 3. Chen DS, et al. Immunity. 2013;39:1-10. 4. Amgen Pipeline. https://www.amgenpipeline.com. Accessed 9/10/20. 5. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02263508. Accessed 9/10/20. 6. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT04068181. Accessed 9/4/20. 7. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02910557. Accessed 9/10/20. 8. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02509507. Accessed 9/10/20. 9. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT02756845. Accessed 9/10/20. 10. ClinicalTrials.gov. https://www.clinicaltrials.gov/ct2/show/NCT03256344. Accessed 9/10/20.

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