This material reflects the GSK research pipeline as of
November 15, 2023
Pipeline
Our unique R&D approach of Science x Technology x Culture is helping to fight cancer on multiple groundbreaking fronts - focusing on maximizing survival through the discovery and development of novel oncology medicines that may have life-changing potential.
Immuno-Oncology
Harnessing The Body’s Immune System
The growing understanding of tumor cells' ability to evade immune surveillance has led to advances in the field of immuno-oncology.1
Malignant cells manipulate a variety of physiological mechanisms involved in antigenicity, immune activation, T-cell priming and recruitment, and upregulation of checkpoint molecules.1 Many of these mechanisms may be impacted simultaneously to promote tumor cell survival.1 Immunotherapies harness the body's own immune system to fight cancer by using different immunological pathways to enhance antitumor responses.1,2
GSK is exploring different clinical assets aimed at augmenting the immune response, reducing immune suppression, and modulating the tumor microenvironment.3,4
Tumor Cell Targeting
Targeting Cancer Cell-Specific Alterations
Cancer cells exhibit differences from somatic cells due to alterations that promote growth, proliferation, survival, and metastasis.5 These tumor-specific attributes can be selectively targeted through established modalities such as antibody-drug conjugates (ADCs); small molecules, like Janus kinase (JAK) and bone morphogenetic protein receptor kinase activin A receptor, type I (ACVR1) inhibitors; and other biological therapies.5-8 GSK is investigating multiple targeted cell therapies in ongoing clinical studies.9
Synthetic Lethality
Inhibiting pathways that contribute to aberrant DNA repair and cellular metabolism
Accumulation of DNA damage, genomic instability, and altered cellular metabolism are pervasive characteristics of human tumors.10-12 Disruption of essential DNA damage repair or cellular metabolism in cancer cells may increase dependency on alternate repair pathways for cell survival or make tumors more susceptible to modulation of metabolic enzymes.11,13 Synthetically lethal therapies aim to combine pharmacologic inhibition of targeted pathways with tumor-inherent defects in key cellular processes that promote aberrant proliferation to selectively kill tumor cells while sparing healthy tissue.11,13-15 GSK is investigating clinical assets that utilize the power of synthetically lethal interactions to fight malignant cells in a variety of cancers.9
Footnotes
£Not yet recruiting as of April 10, 2023.
ᶳIn collaboration with ENGOT, the European Network for Gynaecological Oncological Trial groups.
‡The trial is no longer enrolling patients with endometrial cancer.
~This trial is only enrolling patients for Cohort 2E in NSCLC
§Collaboration and License Alliance between GSK and iTeos Therapeutics.
*In-license or other partnership with third party.
†Collaboration between GSK and Tempus.
1L, first line; ACVR1, bone morphogenetic protein receptor kinase activin A receptor, type I; AML, acute myeloid leukemia; ASCT, autologous stem cell transplant; BCMA, B-cell maturation antigen; CD, cluster of differentiation; dMMR/MSI-H, mismatch repair deficient/microsatellite instability-high; DVd, daratumumab + bortezomib + dexamethasone; ET, essential thrombocythemia; FOLFIRI, folinic acid/leucovorin + 5 fluorouracil + irinotecan; HR-MDS, high-risk myelodysplastic syndrome; IgG1, immunoglobulin G1; JAK1/2, Janus kinase 1/2; mFOLFOX6, modified folinic acid/leucovorin; newly diagnosed multiple myeloma; NSCLC, non-small cell lung cancer; PALB2, partner and localizer of BRCA2; PARP, poly ADP ribose polymerase; Pd, pomalidomide + dexamethasone; PD 1, programmed cell death protein 1; PD-L1, programmed cell death ligand 1; PMF, primary myelofibrosis; PV, polycythemia vera; PVd, pomalidomide + bortezomib + dexamethasone; PVRIG, poliovirus receptor–related immunoglobulin; Rd, lenalidomide + dexamethasone; RRMM, relapsed/refractory multiple myeloma; TIGIT, T-cell immunoreceptor with Ig and ITIM domains; Vd, bortezomib + dexamethasone; VRd, bortezomib + lenalidomide + dexamethasone.
This document contains information for healthcare providers and is intended solely for educational purposes. This display includes ongoing clinical trials for both approved and investigational compounds. Some agents are approved in select indications. Inclusion in this display does not imply regulatory approval for these compounds or all indications. Information about all trials can be found at www.clinicaltrials.gov. All clinical study information updated as of April 10, 2023.
References
- Allard B et al. Semin Cancer Biol. 2018;52(pt 2):1‑11. doi:10.1016/j.semcancer.2018.02.005.
- PhRMA. Medicines in development for immuno-oncology 2017 report. Accessed January 27, 2021. https://phrma.org/-/media/Project/PhRMA/PhRMA-Org/PhRMA-Org/PDF/MID-Reports/MID-Report-Immuno_Oncology-2017.PDF
- Tai YT, Anderson KC. Immunotherapy. 2015;7(11):1187-1199.
- Kumar S et al. MAbs. 2021;13(1):1954136. doi:10.1080/19420862.2021.1954136.
- Lee YT et al. Eur J Pharmacol. 2018;834:188-196.
- Hafeez U et al. Molecules. 2020;25(20):4764. doi:10.3390/molecules25204764
- Levavi H et al. Clin Adv Hematol Oncol. 2022;20(7):456-467.
- Asshoff M et al. Blood. 2017;129(13):1823-1830.
- ClinicalTrials.gov. Accessed April 10, 2023. www.clinicaltrials.gov/
- Lord CJ, Ashworth A. Nature. 2012;481(7381):287-294.
- O’Connor MJ. Mol Cell. 2015;60(4):547-560
- Coller HA. Am J Pathol. 2014;184(1):4-17.
- Marjon K et al. Cell Rep. 2016;15(3):574-587.
- Kelley MR et al. Future Oncol. 2014;10(7):1215-1237
- O’Neil NJ, Bailey ML, Hieter P. Synthetic lethality and cancer. Nat Rev Genet. 2017;18(10):613-623.
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SE-GBL-ON-WCNT-200001 | November 2023