ArticleMolecular cancer therapeutics2022
Targeting CD73 with AB680 (Quemliclustat), a Novel and Potent Small-Molecule CD73 Inhibitor, Restores Immune Functionality and Facilitates Antitumor Immunity.
Article in Molecular cancer therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Metabolomics and metabolites in cancer diagnosis and treatment.Molecular biomedicine · 2025Pooled it
- Quemliclustat and chemotherapy with or without zimberelimab in metastatic pancreatic adenocarcinoma: a randomized phase 1 trial.Nature medicine · 2026Trial
- Differential expression, activity, and fibroblast growth factor 2-mediated modulation of purine-metabolizing enzymes in cultured cortical astrocytes and microglia.Purinergic signalling · 2026Article
- Immunosuppressive Pathways in Cutaneous Melanoma: Functional Integration Between PD-1 and CD73 and Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2026Review
- GBP5 Aggravates Acute Lung Injury Via NLRP3 Inflammasome Activation While Inducing a HIF-1α-CD73-adenosine Feedback Loop.Inflammation · 2026Article
- Fluorine-18-Labeled Nucleotide Analogs Targeting Ecto-5'-Nucleotidase (CD73) for Positron Emission Tomography Imaging of Solid Tumors.Angewandte Chemie (International ed. in English) · 2026Article
- Review
- Potent Competitive Inhibitors of Ecto-5'-nucleotidase (CD73) based on 6‑(Het)aryl-7-deazapurine Ribonucleoside 5'‑ACS pharmacology & translational science · 2026Article
- Dual-mechanism anti-CD73 antibodies CR201 and CR202 targeting distinct domains for cancer immunotherapy.Frontiers in immunology · 2026Article
- Metabolic reprogramming networks in the gastric cancer tumor microenvironment: an integrated axis of nutrient competition, metabolic crosstalk, and immunosuppression.Frontiers in immunology · 2026Review
- Adenosine signaling in tumor immune escape: metabolic checkpoints, myeloid suppression, and combination immunotherapy.Frontiers in oncology · 2026Review
- The CD73-adenosine axis in melanoma: from multidimensional regulation to precision immunotherapy.Frontiers in immunology · 2026Review
- Dual MAO A and HSP90 inhibitors enhance anti-PD-1 therapy and suppress colorectal cancer.Frontiers in pharmacology · 2026Article
- Nanomedicines Reshape the Tumor Microenvironment: Multidimensional Strategies from Modulating "Barriers" to Metabolic Intervention.International journal of nanomedicine · 2026Review
- Metabolomic and transcriptomic profiling of HNSCC identifies AMIGO2 as a therapeutic target modulating tumor microenvironment.NPJ precision oncology · 2025Article
- Purin Metabolism Is Crucial for Regulatory T Cell Stability and Function.European journal of immunology · 2025Review
- Metabolites as agents and targets for cancer immunotherapy.Nature reviews. Drug discovery · 2025Review
- Purinergic pathways and their clinical use in the treatment of acute myeloid leukemia.Purinergic signalling · 2025Review
- Review
- The interaction of AB-680, a CD73 inhibitor, with NBTI, a nucleoside transporter inhibitor, on the adenosinergic control of atrial contractility.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cells play a critical role in the control of cancer. The development of immune checkpoint blockers (ICB) aimed at enhancing antitumor T-cell responses has revolutionized cancer treatment. However, durable clinical benefit is observed in only a subset of patients, prompting research efforts to focus on strategies that target multiple inhibitory signals within the tumor microenvironment (TME) to limit tumor evasion and improve patient outcomes. Adenosine has emerged as a potent immune suppressant within the TME, and CD73 is the major enzyme responsible for its extracellular production. CD73 can be co-opted within the TME to impair T-cell-mediated antitumor immunity and promote tumor growth. To target this pathway and block the formation of adenosine, we designed a novel, selective, and potent class of small-molecule inhibitors of CD73, including AB680 (quemliclustat), which is currently being tested in patients with cancer. AB680 effectively restored T-cell proliferation, cytokine secretion, and cytotoxicity that were dampened by the formation of immunosuppressive adenosine by CD73. Furthermore, in an allogeneic mixed lymphocyte reaction where CD73-derived adenosine had a dominant suppressive effect in the presence of PD-1 blockade, AB680 restored T-cell activation and function. Finally, in a preclinical mouse model of melanoma, AB680 inhibited CD73 in the TME and increased the antitumor activity of PD-1 blockade. Collectively, these data provide a rationale for the inhibition of CD73 with AB680 in combination with ICB, such as anti-PD-1, to improve cancer patient outcomes.
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