Evidence map›Paper›PMID 35849084›Full record

ArticleCancer science2022

Combination therapy with anamorelin and a myostatin inhibitor is advantageous for cancer cachexia in a mouse model.

Kako Hanada, Kunpei Fukasawa, Hiroki Hinata, Shú Imai, Kentaro Takayama, Hideyo Hirai, Rina Ohfusa, Yoshio Hayashi, Fumiko Itoh

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. The causes of cachexia: key signals and the brain.Nature reviews. Endocrinology · 2026
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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

9 authors at 1 institution in 1 country.

Kako HanadaLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Kunpei FukasawaLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Hiroki HinataLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Shú ImaiLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Kentaro TakayamaDepartment of Medicinal Chemistry, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Hideyo HiraiLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Rina OhfusaDepartment of Medicinal Chemistry, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Yoshio HayashiDepartment of Medicinal Chemistry, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Fumiko ItohLaboratory of Stem Cell Regulation, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.ORCID https://orcid.org/0000-0002-6134-5331
Tokyo University of Pharmacy and Life Sciences · JP

Funding

Japanese Ministry of Education, Culture, Sports, Science, and Technology 20K07430
6 · The paper itself

Abstract

Cancer cachexia is a multifactorial disease that causes continuous skeletal muscle wasting. Thereby, it seems to be a key determinant of cancer-related death. Although anamorelin, a ghrelin receptor agonist, has been approved in Japan for the treatment of cachexia, few medical treatments for cancer cachexia are currently available. Myostatin (MSTN)/growth differentiation factor 8, which belongs to the transforming growth factor-β family, is a negative regulator of skeletal muscle mass, and inhibition of MSTN signaling is expected to be a therapeutic target for muscle-wasting diseases. Indeed, we have reported that peptide-2, an MSTN-inhibiting peptide from the MSTN prodomain, alleviates muscle wasting due to cancer cachexia. Herein, we evaluated the therapeutic benefit of myostatin inhibitory D-peptide-35 (MID-35), whose stability and activity were more improved than those of peptide-2 in cancer cachexia model mice. The biologic effects of MID-35 were better than those of peptide-2. Intramuscular administration of MID-35 effectively alleviated skeletal muscle atrophy in cachexia model mice, and the combination therapy of MID-35 with anamorelin increased food intake and maximized grip strength, resulting in longer survival. Our results suggest that this combination might be a novel therapeutic tool to suppress muscle wasting in cancer cachexia.

Indexed as

Biological ProductsNeoplasmsAnimalsCachexiaDisease Models, AnimalHydrazinesMiceMuscle, SkeletalMuscular AtrophyMyostatinOligopeptidesPeptidesReceptors, GhrelinTransforming Growth FactorsanamorelinBiological ProductsHydrazinesMyostatinOligopeptidesPeptidesReceptors, GhrelinTransforming Growth Factorsanamorelincancer cachexiamuscle wastingmyostatin

Identifiers

PMID35849084
PMCPMC9530881
OpenAlexW4285801713

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.