Boger's lab proposed a new and potent class of TLRs agonists -diprovocims . They obtained results from a compound library designed to promote cell surface receptor dimerisation. The revealed mechanism of action was that diprovicims act by inducing cell surface TLR2 dimerisation and activation with TLR1. Later, the basis of TLR2/TLR1 activation by Diprovocim was studied by Su et al. . They combined structural data with MD simulations, MM-PBSA, MM-GBSA binding free energy and mutagenesis analyses, and they showed that the new modulator interacts with TLR2/TLR1 at the same binding pocket as Pam3CSK4. However, the observed conformations around the ligand binding sites were different. The authors noticed the widespread hydrophobic interactions and a hydrogen-bonding network between the receptor and Diprovocim molecules within the ligand binding pocket, which is probably in correlation with the high potency of the discovered compound.