Evidence map›Paper›PMID 33146056›Full record

ArticlemAbs

Fully human anti-CD39 antibody potently inhibits ATPase activity in cancer cells via uncompetitive allosteric mechanism.

Bradley N Spatola, Alana G Lerner, Clifford Wong, Tracy Dela Cruz, Megan Welch, Wanchi Fung, Maria Kovalenko, Karolina Losenkova, Gennady G Yegutkin, Courtney Beers and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in mAbs. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  7. Targeting CD39 as a Therapeutic for Cancer Immunotherapy.Expert reviews in molecular medicine · 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

12 authors at 5 institutions in 2 countries.

Bradley N SpatolaAntibody Development, Tizona Therapeutics , South San Francisco, CA, USA.
Alana G LernerImmunology, Tizona Therapeutics , South San Francisco, CA, USA.
Clifford WongAntibody Development, Tizona Therapeutics , South San Francisco, CA, USA.
Tracy Dela CruzImmunology, Tizona Therapeutics , South San Francisco, CA, USA.
Megan WelchImmunology, Tizona Therapeutics , South San Francisco, CA, USA.
Wanchi FungAntibody Development, Tizona Therapeutics , South San Francisco, CA, USA.
Maria KovalenkoClinical Biomarkers, AbbVie, Redwood City , CA, USA.
Karolina LosenkovaMediCity Research Laboratory, University of Turku , Turku, Finland.
Gennady G YegutkinMediCity Research Laboratory, University of Turku , Turku, Finland.
Courtney BeersImmunology, Tizona Therapeutics , South San Francisco, CA, USA.
John CorbinAntibody Development, Tizona Therapeutics , South San Francisco, CA, USA.
Vanessa B SorosAntibody Development, Tizona Therapeutics , South San Francisco, CA, USA.
Research & Diagnostic Antibodies (United States) · USHorizon Therapeutics (United States) · USUniversity of Turku · FIAbbVie (United States) · USRapt Therapeutics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extracellular ATP/adenosine axis in the tumor microenvironment (TME) has emerged as an important immune-regulatory pathway. Nucleoside triphosphate diphosphohydrolase-1 (NTPDase1), otherwise known as CD39, is highly expressed in the TME, both on infiltrating immune cells and tumor cells across a broad set of cancer indications. CD39 processes pro-inflammatory extracellular ATP to ADP and AMP, which is then processed by Ecto-5'-nucleotidase/CD73 to immunosuppressive adenosine. Directly inhibiting the enzymatic function of CD39 via an antibody has the potential to unleash an immune-mediated anti-tumor response via two mechanisms: 1) increasing the availability of immunostimulatory extracellular ATP released by damaged and/or dying cells, and 2) reducing the generation and accumulation of suppressive adenosine within the TME. Tizona Therapeutics has engineered a novel first-in-class fully human anti-CD39 antibody, TTX-030, that directly inhibits CD39 ATPase enzymatic function with sub-nanomolar potency. Further characterization of the mechanism of inhibition by TTX-030 using CD39

Indexed as

Adenosine TriphosphatasesAntibodies, MonoclonalAntibody AffinityAntineoplastic AgentsApyraseBinding Sites, AntibodyCell Line, TumorEnzyme InhibitorsHumansAdenosine TriphosphatasesAntibodies, MonoclonalAntineoplastic AgentsApyraseENTPD1 protein, humanEnzyme Inhibitorsallosteric regulationATPcancercancer therapyCD39enzyme inhibitorenzyme kineticsenzyme mechanismmonoclonal antibody

Identifiers

PMID33146056
PMCPMC7646477
OpenAlexW3096779319

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.