Development of Mitochondria-Targeted PARP Inhibitors.

Pavels Dimitrijevs, Marina Makrecka-Kuka, Pavel Arsenyan

Abstract read

In one paragraph

Article in Biomolecules, 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

3 authors.

Pavels DimitrijevsLatvian Institute of Organic Synthesis, Aizkraukles 21, LV1006 Riga, Latvia.ORCID 0000-0002-6332-2395

Marina Makrecka-KukaLatvian Institute of Organic Synthesis, Aizkraukles 21, LV1006 Riga, Latvia.ORCID 0000-0003-4549-1993

Pavel ArsenyanLatvian Institute of Organic Synthesis, Aizkraukles 21, LV1006 Riga, Latvia.ORCID 0000-0001-5875-2799

Funding

RRF project No.5.2.1.1.i.0/2/24/I/CFLA/001 07/OSI/ZG

6 · The paper itself

Abstract

PARP inhibitors are a clinically validated class of anticancer therapeutics that exploit synthetic lethality to target homologous recombination-deficient tumors, such as those carrying BRCA1/2 mutations. Nevertheless, the rational design of mitochondria-targeted PARP inhibitors capable of selective mitochondrial accumulation and organelle-specific PARP modulation remains an unresolved objective. To enable organelle-specific modulation of PARP activity, we synthesized a series of trialkyl(aryl)phosphonium conjugates of olaparib and rucaparib designed to target mitochondria by cardiolipin binding. Their activity was evaluated by PARP1 inhibition, cardiolipin affinity, and cytotoxicity in BRCA1-deficient HCC1937 breast cancer cells and non-malignant H9C2 cardiomyocytes. All conjugates retained potent PARP1 inhibition (IC

Indexed as

Antineoplastic AgentsMitochondriaPoly(ADP-ribose) Polymerase InhibitorsAnimalsCardiolipinsCell Line, TumorHumansIndolesPhthalazinesPiperazinesPoly (ADP-Ribose) Polymerase-1Antineoplastic AgentsCardiolipinsIndolesolaparibPhthalazinesPiperazinesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase Inhibitorsrucaparibcardiolipin bindingmitochondrial targetingolaparibPARP inhibitorsphosphonium conjugatesrucaparib

Identifiers

PMID41594705

DOI10.3390/biom16010165

PMCPMC12839213

What Socratic holds

Textmetadata

LicenceCC BY

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 Socratic graph.