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. 2020 Mar 6;170(5):104–111. doi: 10.1007/s10354-020-00741-6

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Drugs in development for the treatment of achondroplasia. Depicted is a growth plate chondrocyte. The main targets are FGFR3 ligands, the mutated FGFR3 and its activated downstream MAPK signalling pathway, as well as the NPR‑B receptor. In bold are substances currently in clinical trials (as of November 30, 2019). The complex MAPK pathway which originates from FGFR3, as well the MAPK-inhibitory pathway that originates from NPR‑B activation, are depicted for simplification