Evidence map›Paper›PMID 41606188›Full record

ArticleCommunications medicine2026

Selective blockade of latent TGF-β1 activation suppresses tissue fibrosis with good safety.

Masakazu Kanamori, Izumi Sato, Christine Xing'er Koo, Yang Sun, Hiroki Kawauchi, Kenji Nakagawa, Atsuko Murai, Kentaro Asanuma, Siok Wan Gan, Chai Ling Pang and 10 more

Abstract read
In one paragraph

Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

20 authors.

Masakazu Kanamori *Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Izumi Sato *Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.ORCID http://orcid.org/0000-0002-1770-0260
Christine Xing'er KooChugai Pharmabody Research Pte. Ltd., Singapore, Singapore.
Yang SunChugai Pharmabody Research Pte. Ltd., Singapore, Singapore.
Hiroki KawauchiResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Kenji NakagawaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.ORCID http://orcid.org/0009-0002-1894-2285
Atsuko MuraiTranslational Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Kentaro AsanumaTranslational Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Siok Wan GanChugai Pharmabody Research Pte. Ltd., Singapore, Singapore.
Chai Ling PangChugai Pharmabody Research Pte. Ltd., Singapore, Singapore.
Yuichiro ShimizuResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Meiri Shida-KawazoeResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Chisako KanamaruTranslational Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Yoko KayukawaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Natsuko HadaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Ken OhmineTranslational Research Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Takehisa KitazawaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.ORCID http://orcid.org/0000-0002-4958-7936
Junichi NezuResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.
Tomoyuki IgawaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan.ORCID http://orcid.org/0000-0003-0097-8220
Hideaki ShimadaResearch Division, Chugai Pharmaceutical Co. Ltd., Yokohama, Kanagawa, Japan. shimada.hideaki12@chugai-pharm.co.jp.ORCID http://orcid.org/0000-0003-4932-1385

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibrosis is a hallmark of organ failure observed after chronic epithelial injury and inflammation. The transforming growth factor beta (TGF-β) is the master regulator of fibrogenesis, so blockade of the TGF-β pathway is a potential treatment strategy for fibrosis; however, the therapeutic potential of pan-TGF-β blockade is limited by side effects.

methodsWe generated SOF10, a humanized antibody that targets latent TGF-β1 and selectively blocks protease- and integrin αvβ8-mediated latent TGF-β1 activation. We conducted gene expression and histological analyses in nonalcoholic steatohepatitis (NASH)/liver fibrosis and renal interstitial fibrosis models. We also evaluated the combination effect of SOF10 with an immune checkpoint inhibitor in a syngeneic mouse model and performed safety studies in mice and monkeys.

resultsHere we show that SOF10 reduces fibrosis in NASH/liver fibrosis and renal interstitial fibrosis models and improves renal function in a chronic kidney disease model. Furthermore, the combination of SOF10 with an anti-PD-L1 antibody decreases tumor growth in a syngeneic mouse model. SOF10 demonstrates safety in both mice and monkeys.

conclusionsSelective blockade of latent TGF-β1 activation represents a promising approach for treating a broad range of fibrotic diseases and cancers. By specifically targeting TGF-β1, SOF10 may offer a safer and more effective therapeutic option compared to non-selective TGF-β inhibitors. This strategy has the potential to transform the treatment paradigm for fibrosis-related conditions.

Identifiers

PMID41606188
PMCPMC12953895

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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.