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Cocktail and Poster Display session

47P - Unlocking potential for enhancing anti-tumor immunity: Targeting hematopoietic progenitor kinase 1 (HPK1) with novel small molecules

Date

26 Feb 2024

Session

Cocktail and Poster Display session

Topics

Targeted Therapy

Tumour Site

Presenters

Sreevalli Sharma

Citation

Annals of Oncology (2024) 9 (suppl_1): 1-11. 10.1016/esmoop/esmoop102271

Authors

S.V. Sharma1, R. Rao2, S. Venkatesan3, H. Kaushik Kotakonda4, S. Sarma1, D. Pillai1, S. Reddy4, K. Thoppe Siraja1, N. Belugali Nataraj1, N. Katagihallimath5, S. Hameed P6

Author affiliations

  • 1 R&d Cell And Molecular Biology, Bugworks Research India Pvt. Ltd., 560065 - Bengaluru/IN
  • 2 R&d Chemistry, Bugworks Research India Pvt. Ltd., 560065 - Bengaluru/IN
  • 3 R&d System Biology, Bugworks Research India Pvt. Ltd., 560065 - Bengaluru/IN
  • 4 R&d Dmpk, Bugworks Research India Pvt. Ltd., 560065 - Bengaluru/IN
  • 5 R&d Biochemistry, Bugworks Research India Pvt Ltd, 560065 - Bengaluru/IN
  • 6 R&d Medicinal Chemistry, Bugworks Research India Pvt. Ltd., 560065 - Bengaluru/IN

Resources

This content is available to ESMO members and event participants.

Abstract 47P

Background

HPK1, a MAP4K family serine/threonine kinase exclusive to hematopoietic cells, plays a pivotal role in dampening TCR and BCR signal cascades. Its functions extend to influencing IL2 secretion, T-cell maturation and migration, tumor infiltration and dendritic cell antigen presentation. Targeting HPK1 with small molecules presents a promising approach to enhance antitumor immunity.

Methods

Structure-guided medicinal chemistry was used to design and optimize the potency against HPK1 kinase and selectivity against the MAP4K family using a panel of enzymatic assays. Target engagement and immune activation were assessed by monitoring phosphorylated SLP76, which is a key target of HPK1 in the T-cell receptor complex and pharmacological inhibition of HPK1, leading to T-cell activation and cytokine secretion. Syngeneic mouse models were used to demonstrate that the molecules are orally bioavailable and can inhibit tumor growth.

Results

Bugworks identified BWC4642 and BWC4496 as optimized leads with an IC50 of <1 nM against HPK1 and a >30-fold selectivity window against MAP4K2, MAP4K3, MAP4K4, MAP4K5, and MAP4K6. Both compounds effectively inhibit SLP76 phosphorylation in human blood, indicating target engagement. They restore immune function by reversing the suppression of IL2 and IFNγ secretion mediated by prostaglandin E2/adenosine in human PBMCs, implying T cell activation. The lead compounds exhibited significant tumor killing as stand-alone or in combination with selected FDA-approved drugs in co-culture assays of tumor cells and PBMC. Early lead compounds (BWC3304) demonstrated good oral bioavailability and in vivo efficacy by inhibiting tumor growth as a single agent and in combination with anti-PD1 therapy in the syngeneic MCA-205 mouse model.

Conclusions

The identified novel leads are potent, selective, and orally bioavailable HPK1 inhibitors that demonstrate efficacy in suppressing tumor growth and enhancing the anti-tumor immune response. Thus, they are a potential therapeutic option for augmenting immunotherapy for several types of cancer. Further preclinical and clinical studies are warranted to validate their potential as a therapeutic option for cancer patients.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Bugworks Research India Pvt. Ltd.

Funding

Bugworks Research India Pvt. Ltd.

Disclosure

S. Sharma, R. Rao, S. Venkatesan, H. Kaushik Kotakonda, S. Sarma, D. Pillai, S. Reddy, K. Thoppe Siraja, N. Belugali Nataraj, N. Katagihallimath: Financial Interests, Personal, Stocks/Shares: Bugworks Research India Pvt Ltd. S. Hameed P: Financial Interests, Personal, Stocks/Shares: Bugworks Research India Pvt Ltd.; Financial Interests, Institutional, Other, Chief Scientific Officer: Bugworks Research India Pvt Ltd.

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