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Using a total of 9.0 fb −1 of e + e − collision data with center-of-mass energies between 4.15 and 4.30 GeV collected by the BESIII detector, we search for the processes e + e − → γX(3872) with X(3872) → π 0 χcJ for J = 0, 1, 2. We report the first observation of X(3872) → π 0 χc1, a new decay mode of the X(3872), with a statistical significance of more than 5σ. Normalizing to the previously established process e + e − → γX(3872) with X(3872) → π + π − J/ψ, we find B(X(3872) → π 0 χc1)/B(X(3872) → π + π − J/ψ) = 0.88 +0.33 −0.27 ±0.10, where the first error is statistical and the second is systematic. We set 90% confidence level upper limits on the corresponding ratios for the decays to π 0 χc0 and π 0 χc2 of 19 and 1.1, respectively.

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Coronaviruses (CoVs) are positive single‐stranded RNA viruses that cause severe respiratory syndromes in humans, including severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Coronavirus disease 2019 (COVID‐19) caused by a novel severe acute respiratory syndrome CoV (SARS‐CoV‐2) at the end of 2019 became a global pandemic. The 3C‐like cysteine protease (3CLpro) processes viral polyproteins to yield mature non‐structural proteins, thus playing an important role in the CoV life cycle, and therefore is considered as a prominent target for antiviral drugs. To date, many 3CLpro inhibitors have been reported, and their molecular mechanisms have been illustrated. Here, we briefly introduce the structural features of 3CLpro of the human‐related SARS‐CoV, MERS‐CoV and SARS‐CoV‐2, and explore the potency and mechanism of their cognate inhibitors. This information will shed light on the development and optimization of CoV 3CLpro inhibitors, which may benefit the further designation of therapeutic strategies for treating CoV diseases.