Evidence map›Paper›PMID 42110537›Full record

ReviewFrontiers in pharmacology2026

Phosphoethanolamine: a translational journey from biological process and physiopathological effects to therapeutical innovation - a mini-review.

Guilherme Ayres Rossini, Marcia Koike, Denise F Barbeiro, Hermes Barbeiro, Daniel Rabelo, Francisco Garcia Soriano, Marcel Cerqueira Cesar Machado, Durvanei Augusto Maria

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Guilherme Ayres RossiniMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Marcia KoikeMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Denise F BarbeiroMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Hermes BarbeiroMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Daniel RabeloFaculty of Medicine, University of São Paulo, São Paulo, Brazil.
Francisco Garcia SorianoMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Marcel Cerqueira Cesar MachadoMedical Investigation Laboratory 51 (LIM51) - Clinics Hospital Faculty of Medicine, University of São Paulo (HC-FMUSP), São Paulo, Brazil.
Durvanei Augusto MariaFaculty of Medicine, University of São Paulo, São Paulo, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoethanolamine (pETN), an endogenous metabolite in the Kennedy pathway for membrane phospholipid synthesis, can be chemically synthesized and exemplifies translational pharmacology through its journey from basic biochemistry to clinical application. Initially recognized for phosphatidylethanolamine biosynthesis via PCYT2-mediated conversion, pETN gained clinical attention following reports of Brazilian cancer patients with pETN-containing products. Subsequent pharmacological studies revealed favorable safety profiles in preclinical and clinical settings, with oral bioavailability of 6%-7%. Mechanistic investigations identified pETN as a competitive inhibitor of succinate dehydrogenase (complex II and Krebs cycle), providing molecular rationale for its mitochondrial effects. This discovery opened new therapeutic avenues beyond oncology, particularly in ischemia-reperfusion injury, where pETN's succinate dehydrogenase inhibitory activity could mitigate pathological succinate accumulation and subsequent oxidative damage during reperfusion. The translational trajectory of pETN, from endogenous metabolism through clinical observation to mechanistic understanding, exemplifies the bidirectional nature of modern pharmacological research and positions this naturally occurring compound as a promising therapeutic candidate for mitochondrial dysfunction-related conditions.

Indexed as

2-aminoethyl dihydrogen phosphateETNK1ischemia reperfusion (I/R) injuryPcyt2phosphoethanolaminephospholipid metabolismsuccinate dehydrogenase (complex II)

Identifiers

PMID42110537
PMCPMC13149127

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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.