Evidence map›Paper›PMID 31805108›Full record

ArticlePloS one2019

Fragment-based design of small molecule PCSK9 inhibitors using simulated annealing of chemical potential simulations.

Frank Guarnieri, John L Kulp, John L Kulp, Ian S Cloudsdale

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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

4 authors at 2 institutions in 1 country.

Frank GuarnieriCenter for Drug Discovery, Northeastern University, Boston, MA, United States of America.ORCID 0000-0003-0482-3509
John L KulpConifer Point Pharmaceuticals, Doylestown, PA, United States of America.
John L KulpConifer Point Pharmaceuticals, Doylestown, PA, United States of America.
Ian S CloudsdaleConifer Point Pharmaceuticals, Doylestown, PA, United States of America.
Baruch S. Blumberg Institute · USNortheastern University · US

Funding

An Open Web Service For Fragment-based Design of Small Molecule InhibitorsR44GM109549 · NIGMS · CONIFER POINT PHARMACEUTICALS, LLC · PI John Laurence Kulp III · 2018 to 2026
$3.6M
NIGMS NIH HHS R44 GM109549
6 · The paper itself

Abstract

PCSK9 is a protein secreted by the liver that binds to the low-density lipoprotein receptor (LDLR), causing LDLR internalization, decreasing the clearance of circulating LDL particles. Mutations in PCSK9 that strengthen its interactions with LDLR result in familial hypercholesterolemia (FH) and early onset atherosclerosis, while nonsense mutations of PCSK9 result in cardio-protective hypocholesterolemia. These observations led to PCSK9 inhibition for cholesterol lowering becoming a high-interest therapeutic target, with antibody drugs reaching the market. An orally-available small molecule drug is highly desirable, but inhibiting the PCSK9/LDLR protein-protein interaction (PPI) has proven challenging. Alternate approaches to finding good lead candidates are needed. Motivated by the FH mutation data on PCSK9, we found that modeling the PCSK9/LDLR interface revealed extensive electron delocalization between and within the protein partners. Based on this, we hypothesized that compounds assembled from chemical fragments could achieve the affinity required to inhibit the PCSK9/LDLR PPI if they were selected to interact with PCSK9 in a way that, like LDLR, also involves significant fractional charge transfer to form partially covalent bonds. To identify such fragments, Simulated Annealing of Chemical Potential (SACP) fragment simulations were run on multiple PCSK9 structures, using optimized partial charges for the protein. We designed a small molecule, composed of several fragments, predicted to interact at two sites on the PCSK9. This compound inhibits the PPI with 1 μM affinity. Further, we designed two similar small molecules where one allows charge delocalization though a linker and the other doesn't. The first inhibitor with charge delocalization enhances LDLR surface expression by 60% at 10 nM, two orders of magnitude more potent than the EGF domain of LDLR. The other enhances LDLR expression by only 50% at 1 μM. This supports our conjecture that fragments can have surprisingly outsized efficacy in breaking PPI's by achieving fractional charge transfer leading to partially covalent bonding.

Indexed as

Computer SimulationDrug DesignPCSK9 InhibitorsAcetyleneBenzimidazolesBinding, CompetitiveEnzyme AssaysEnzyme InhibitorsHep G2 CellsHumansModels, MolecularProprotein Convertase 9Protein BindingProtein Interaction MapsReceptors, LDLRotationAcetylenebenzimidazoleBenzimidazolesEnzyme InhibitorsPCSK9 InhibitorsProprotein Convertase 9Receptors, LDLSmall Molecule Libraries

Identifiers

PMID31805108
PMCPMC6894869
OpenAlexW2993037236

What OpenQuestion 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 OpenQuestion graph.