We present recent progress in using molecular modelling as a guide for designing ultra-stable, backbone-cyclic peptides for biotechnological applications. Especially, we focus on peptide engineering strategies in which (1) structured peptides are backbone-cyclised or (2) linear peptides are stabilised by grafting in a cyclic scaffold. In general, the computational design process involves modifying the sequence of cyclic peptides for optimising their interactions with molecular targets using structural bioinformatics algorithms and molecular dynamics (MD) simulations. Basic structural models are typically employed at an early stage for determining the minimal size of the cyclising linker so that the fold and binding mode of a structured peptide are minimally affected by cyclization. For example, we used MD simulations and then mutagenesis to determine why the cyclisation of the potassium channel blocker PVIIA disrupted an important electrostatic interaction with the pore of the channel. In another study, we simplified the structure of cyclic α-conotoxin Vc1.1 while preserving most of its activity at nicotinic acetylcholine receptors. Regarding grafting linear epitopes in cyclic scaffolds, molecular modelling could be used to suggest recipient loops as well as the nature and size of flanking linkers. As an application, we showed that the conformational stability measured during MD simulations of the binding mode of grafted inhibitors of ABL kinase, a leukaemia target, correlated with their potency. The number of natural, ultra-stable, cyclic scaffolds that could be used for grafting is limited. We participated in the creation of a new computational approach for the de novo design of cyclic scaffolds. Starting from the desired topology, a peptide sequence is optimised for the target fold with the Rosetta modelling framework. Using this method, six highly-stable cyclic peptides displaying various combinations of helix and strands elements were designed, and their predicted structures were supported by NMR spectroscopy.