Evidence map›Paper›PMID 40567374›Full record

ReviewFrontiers in pharmacology2025

Tiragolumab and TIGIT: pioneering the next era of cancer immunotherapy.

Kosar Ghasemi

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed.

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  7. Timing matters: how mechanism-guided sequencing shapes the efficacy of radiotherapy-immunotherapy combinations : A systematic review.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
    Review
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  9. SMARCA4-Directed Treatment in Oncology Clinical Trials: A Review.Journal of immunotherapy and precision oncology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Kosar GhasemiDepartment of Pharmacology and Toxicology, School of Pharmacy, Jundishapur University of Medical Sciences, Ahvaz, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tiragolumab, a monoclonal antibody (mAb) targeting T cell immunoreceptor with Ig and ITIM domains (TIGIT), represents a novel approach in cancer immunotherapy. TIGIT, an immunological checkpoint receptor, suppresses T cell activation and promotes immune evasion in various cancers. By inhibiting TIGIT, Tiragolumab enhances T cell-mediated anti-tumor immunity, particularly when combined with programmed cell death-1 (PD-1) and programmed death-ligand 1 (PD-L1) inhibitors. This synergy arises from complementary mechanisms, where TIGIT blockade reduces CD155-mediated suppression, amplifying PD-1/PD-L1-driven T cell activation. Phase II and III trials, including the CITYSCAPE trial for non-small cell lung cancer (NSCLC), have shown improved objective response rates (37% vs. 21% with PD-L1 inhibitor monotherapy) and progression-free survival (PFS), with manageable adverse effects. However, the potential of other checkpoint inhibitors, such as Lymphocyte Activation Gene 3 (LAG3), T-cell immunoglobulin and mucin domain-3 (TIM-3), or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), remains underexplored compared to TIGIT. This review summarizes TIGIT's molecular mechanisms, preclinical and clinical data, and limitations, including resistance mechanisms (e.g., upregulation of alternative checkpoints), biomarker development, and the need for broader investigation into alternative inhibitors to optimize combination therapies for personalized, durable cancer treatment.

Indexed as

cancercancer immunotherapyimmune checkpoint inhibitor 19TIGITtiragolumab

Identifiers

PMID40567374
PMCPMC12187662

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.