Evidence map›Paper›PMID 42563406›Full record

ArticleEndocrinology2026

Development and characterization of a long-acting allosteric growth hormone receptor antagonist for acromegaly.

Katherine Kurylo, Page R Bouchard, Mark N Milton, Peter F Moesta, Laura E Dichtel, Jesper Gromada, Vyas Ramanan, Thomas Vincent, Melinda Smith, Chew Shun Chang and 6 more

Abstract read
In one paragraph

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

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0cells of the map it votes in
0citing papers in PubMed
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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

16 authors.

Katherine KuryloMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0009-0003-7248-5078
Page R BouchardMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0000-0002-5528-1941
Mark N MiltonMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0009-0008-0972-0908
Peter F MoestaMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0009-0002-3200-5917
Laura E DichtelMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0000-0001-6989-2308
Jesper GromadaMarea Therapeutics, South San Francisco, CA 94080, USA.
Vyas RamananMarea Therapeutics, South San Francisco, CA 94080, USA.
Thomas VincentAlloy Therapeutics, Waltham, MA 02451, USA.
Melinda SmithAlloy Therapeutics, Waltham, MA 02451, USA.
Chew Shun ChangAlloy Therapeutics, Waltham, MA 02451, USA.
Jack McGuireAlloy Therapeutics, Waltham, MA 02451, USA.ORCID 0000-0002-7589-7268
Richard ShimketsAlloy Therapeutics, Waltham, MA 02451, USA.
Mark P JoingMarea Therapeutics, South San Francisco, CA 94080, USA.
Joshua Lehrer-GraiwerMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0009-0006-1196-7307
Beryl B CummingsMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0000-0001-6346-1646
Ethan J WeissMarea Therapeutics, South San Francisco, CA 94080, USA.ORCID 0000-0001-9936-5816

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acromegaly is a rare disease caused by growth hormone (GH) hypersecretion from a pituitary adenoma. Pegvisomant is the only approved GH receptor antagonist (GHRA) and is administered via daily subcutaneous injections, which limits real-world effectiveness. Here, we report the discovery and characterization of MAR002, a novel, half-life extended monoclonal antibody GHRA. MAR002 was identified by immunizing transgenic mice with the extracellular domain of human and cynomolgus monkey GH receptor (GHR) and engineered with Fc modifications to limit effector function and extend serum half-life. MAR002 was benchmarked against pegvisomant in biophysical assays, cellular signaling inhibition studies, and a head-to-head pharmacokinetic/pharmacodynamic study in cynomolgus monkeys. MAR002 exhibited higher binding affinity to GHR and >100-fold more potent inhibition of GH-induced GHR signaling than pegvisomant (human half-maximal inhibitory concentration [IC50] 1.05 nM vs 122 nM). Epitope binning demonstrated simultaneous binding of MAR002 and GH to GHR, consistent with an allosteric, noncompetitive mechanism; notably, MAR002 inhibitory activity was maintained at supraphysiological GH concentrations, whereas pegvisomant activity was competitively reduced. In cynomolgus monkeys, a single 10 mg/kg intravenous dose of MAR002 sustained ≥50% IGF-1 suppression for 36 days compared with 15 days for an equimolar pegvisomant dose, with comparable maximal lowering (∼80%). These findings support clinical evaluation of MAR002 as a next-generation long-acting GHRA for acromegaly, with potential for reduced dosing frequency and more consistent suppression of the GH-IGF-1 axis.

Indexed as

AcromegalyAntibodies, MonoclonalHuman Growth HormoneReceptors, SomatotropinAllosteric RegulationAnimalsFemaleHumansMacaca fascicularisMaleMiceMice, TransgenicSignal TransductionAntibodies, MonoclonalHuman Growth HormonepegvisomantReceptors, Somatotropinacromegalygrowth hormone receptor antagonistIGF-1MAR002pegvisomant

Identifiers

PMID42563406
PMCPMC13481985

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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.