While the binding affinity of complex 1a is around 100-fold lower than that of the existing VHL–HIF-1α inhibitor VH298, we have demonstrated here that administering complex 1a at higher dosages (over 30-fold higher compared to the dosage of VH298 used in a previous study52) and through various routes can lead to a significant accumulation of complex 1a at injured skin tissue and promising wound healing effects in animal models of diabetes (including db/db, HFD/STZ and STZ) without significant toxicity. Here, HIF1A is linked to diabetes mellitus.