Evidence map›Paper›PMID 32568648›Full record

ArticleStroke2020

3K3A-Activated Protein C Variant Does Not Interfere With the Plasma Clot Lysis Activity of Tenecteplase.

Purba Mukherjee, Patrick Lyden, José A Fernández, Thomas P Davis, Kent E Pryor, Berislav V Zlokovic, John H Griffin

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

Article in Stroke, 2020. 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
0.1field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

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

7 authors at 5 institutions in 1 country.

Purba MukherjeeDepartment of Molecular Medicine, Scripps Research Institute, La Jolla, CA (P.M., J.A.F., J.H.G.).
Patrick LydenDepartment of Neurology, Cedars-Sinai Medical Center, Los Angeles, CA (P.L.).
José A FernándezDepartment of Molecular Medicine, Scripps Research Institute, La Jolla, CA (P.M., J.A.F., J.H.G.).
Thomas P DavisDepartment of Medical Pharmacology, University of Arizona, Tucson (T.P.D.).
Kent E PryorZZ Biotech LLC, Houston, TX (K.E.P.).
Berislav V ZlokovicZilkha Neurogenetic Institute, University of Southern California, Los Angeles, CA (B.V.Z.).
John H GriffinDepartment of Molecular Medicine, Scripps Research Institute, La Jolla, CA (P.M., J.A.F., J.H.G.).
Scripps Research Institute · US490 BioTech (United States) · USCedars-Sinai Medical Center · USTucson Medical Center · USUniversity of Southern California · US

Funding

Regulation of Protein C PathwaysR01HL142975 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H, MOSNIER, LAURENT OLIVIER · 2018 to 2025
$7.3M
Thrombin Mediated Cytotoxicity during Cerebral IschemiaR01NS075930 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LYDEN, PATRICK D · 2011 to 2020
$3.6M
Activated protein C system in stroke modelsR01NS090904 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZLOKOVIC, BERISLAV V · 2014 to 2018
$3.2M
The NIH SPAN Coordinating CenterU24NS113452 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LYDEN, PATRICK D · 2019 to 2021
$2.4M
Human exomics genotyping-driven discovery and characterization of proteins related to clinical thrombosis, blood coagulation and thrombin generationR01HL133728 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H · 2016 to 2019
$1.9M
NHLBI NIH HHS R01 HL133728NHLBI NIH HHS R01 HL142975NINDS NIH HHS R01 NS075930NINDS NIH HHS R01 NS090904NINDS NIH HHS U24 NS113452
6 · The paper itself

Abstract

background and purposeA recombinant engineered variant of APC (activated protein C), 3K3A-APC, lacks anticoagulant properties (<10%) while preserving APCs anti-inflammatory, anti-apoptotic, and neuroprotective functions and is very promising in clinical trials for ischemic stroke. Therapeutic intervention with single bolus administration of the third-generation tPA (tissue-type plasminogen activator), tenecteplase, is anticipated to be widely adopted for treatment of acute ischemic stroke. 3K3A-APC is well-tolerated in stroke patients dosed with alteplase, and in vitro studies show 3K3A-APC does not interfere with alteplase-induced clot lysis. The purpose of this in vitro study was to assess the influence of 3K3A-APC on tenecteplase-induced clot lysis.

methodsTenecteplase-mediated lysis of thrombin generated plasma clots of human normal pooled plasma was monitored in the presence of varying doses of 3K3A-APC. The effects on fibrinolysis by tenecteplase and alteplase were compared.

resultsThe presence of 3K3A-APC shortened the time for clot lysis induced by tenecteplase at very low levels but not at higher therapeutic concentrations of tenecteplase. Comparisons of alteplase-mediated clot lysis to tenecteplase clot lysis showed that both thrombolytic agents behaved similarly in the presence of 3K3A-APC.

conclusionsThese results indicate that 3K3A-APC does not interfere with tenecteplase's clot lysis function.

Indexed as

FibrinolysisFibrinolytic AgentsHumansIn Vitro TechniquesProtein CRecombinant ProteinsTenecteplaseThrombosis3K3A-APC proteinFibrinolytic AgentsProtein CRecombinant ProteinsTenecteplaseanticoagulantsfibrinolysisprotein Ctenecteplasetissue-type plasminogen activator

Identifiers

PMID32568648
PMCPMC7380733
OpenAlexW3036121864

What OpenQuestion holds

Textmetadata
LicenceTDM
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.