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. 2023 Apr 17:1–16. Online ahead of print. doi: 10.1038/s41577-023-00856-y

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Fig. 4 — Classic and trans-signalling of interleukin-6 (IL-6) and IL-11 can be inhibited by antagonistic substances (for example, antibodies and small molecules) directed against the cytokine, the α-receptors, or glycoprotein 130 (gp130)-associated Janus kinases (JAKs). Antibodies to gp130 are currently not in clinical development. Trans-signalling is inhibited by variants of soluble gp130. Sgp130Fc (soluble gp130–Fc fusion protein) inhibits IL-6 and IL-11 trans-signalling, chimeric soluble gp130 (cs130) inhibits IL-6 trans-signalling, and the autoinhibitory N-terminal ADAM17 (a disintegrin and metalloproteinase 17) pro-domain (A17pro) inhibits the release of soluble IL-6 receptor (sIL-6R), prevents IL-6 trans-signalling and might increase classic signalling because mIL-6R level might increase. A selective IL-11 trans-signalling inhibitor has not been described. Selective classic-signalling inhibitors have also not been developed thus far.