The Effects Of Recombinant Human Pentraxin-2, (PRM-151), On Circulating Fibrocytes In Idiopathic Pulmonary Fibrosis (IPF)

Getsy, John; harper, dawn; Levy, M.B; Burggraaf, Jacobus; Moerland, Matthijs; Visser, I. De; Wijsenbeek, Marlies; Blink, Bernt van den; Gumbhir‐Shah, Kavita; Cohen, Adam F.; Lupher, Mark L.

doi:10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3803

Cited by 2 publications

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“…Patients with IPF show reduced levels of pentraxin 2 [70]. In a randomised, double-blind, single ascending dose study in healthy volunteers (N ¼ 26), single doses of PRM-151 up to 20 mg/kg were well tolerated, with no dose-limiting adverse events [66]. When a single dose of PRM-151 (10 mg/kg) was administered to 3 patients with IPF, elevated IL-6 levels were reduced, as were circulating fibrocytes [66].…”

Section: Prm-151mentioning

confidence: 99%

“…PRM-151 (Promedior/Bristol-Myers Squibb) is an intravenously administered recombinant form of human pentraxin 2 [66]. Pentraxin 2, also known as serum amyloid P (SAP) or PTX2, is a plasma protein that is a potent inhibitor of fibrocyte differentiation from monocytes/macrophages [67].…”

Section: Prm-151mentioning

confidence: 99%

“…In a randomised, double-blind, single ascending dose study in healthy volunteers (N ¼ 26), single doses of PRM-151 up to 20 mg/kg were well tolerated, with no dose-limiting adverse events [66]. When a single dose of PRM-151 (10 mg/kg) was administered to 3 patients with IPF, elevated IL-6 levels were reduced, as were circulating fibrocytes [66]. In a Phase I randomised, double-blind, placebocontrolled ascending dose study in patients with IPF (N ¼ 21), PRM-151 given on days 1, 3, 5, 8 and 15 was generally well tolerated [71].…”

Section: Prm-151mentioning

confidence: 99%

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Therapeutic targets in idiopathic pulmonary fibrosis

Kolb

Bonella

Wollin

2017

Respiratory Medicine

108

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Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal interstitial lung disease. After many drugs failed in clinical trials, improvements in the understanding of the pathogenesis of IPF led to the approval of two drugs that slow the progression of the disease. However, the prognosis for patients with IPF remains poor and the search continues for drugs that inhibit the pathogenic pathways active in IPF to reduce or even halt the progression of the disease. In this article, we review the mechanisms of action of the two approved therapies for IPF (nintedanib and pirfenidone) and of the investigational compounds that are in Phase II trials and discuss the potential for combination therapy in the treatment of IPF.

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Section: Prm-151mentioning

confidence: 99%

Section: Prm-151mentioning

confidence: 99%