Mode of disease/Mode of action
MOD
PDE4B is a central amplifier of fibrosis, immune dysregulation, and vascular instability in pulmonary fibrosis1-3
5’AMP, adenosine 5'-monophosphate; cAMP, cyclic adenosine monophosphate; ECM, extracellular matrix; MOA, mechanism of action; MOD, mechanism of disease; PDE, phosphodiesterase.
MOA
JASCAYD® is a preferential PDE4B inhibitor with antifibrotic, immunomodulatory, and vascular effects2,3
IFN, interferon; IL, interleukin; TNF, tumor necrosis factor.
MOA VIDEO
Watch the video below for an in-depth look at the mechanism of action of JASCAYD®
*Results demonstrated in preclinical animal and in vitro human models.3
Quicklinks
References
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Kolb M, Crestani B, Maher TM. Phosphodiesterase 4B inhibition: a potential novel strategy for treating pulmonary fibrosis. Eur Respir Rev. 2023;32(167):220206.
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Reininger D, Wolf F, Mayr CH, et al. Insights into the cellular and molecular mechanisms behind the antifibrotic effects of nerandomilast. Am J Respir Cell Mol Biol. 2025;73(5):700-712.
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Herrmann FE, Hesslinger C, Wollin L, Nickolaus P. BI 1015550 is a PDE4B inhibitor and a clinical drug candidate for the oral treatment of idiopathic pulmonary fibrosis. Front Pharmacol. 2022;13:838449.
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Fan T, Wang W, Wang Y, et al. PDE4 inhibitors: potential protective effects in inflammation and vascular diseases. Front Pharmacol. 2024;15:1407871.
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Peter D, Jin SLC, Conti M, Hatzelmann A, Zitt C. Differential expression and function of phosphodiesterase 4 (PDE4) subtypes in human primary CD4+ T cells: predominant role of PDE4D. J Immunol. 2007;178:4820-4831.
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Li H, Zuo J, Tang W. Phosphodiesterase-4 inhibitors for the treatment of inflammatory diseases. Front Pharmacol. 2018;9:1048.
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JASCAYD® UAE Local SmPC; May 2026.
MLR ID: PC-AE-102896
Expiry Date: 10/05/2028