The effect of deuteration on relaxation rates in cartilage is expected to be similar. Both the isotropic and anisotropic contributions to transverse relaxation are expected to be affected, although, the behaviour, in particular, of the anisotropic contribution to T2 relaxation is of foremost interest to us. In this paper, we present the results from our study of proton spin relaxation behaviour in bovine articular cartilage in the presence of deuterium oxide. We examined the longitudinal relaxation rates and the isotropic and anisotropic contributions to transverse relaxation rates, and their response to increasing levels of deuteration in cartilage. We anticipated significant decrease in the relaxation rates with increasing deuterium concentrations. Our results revealed unexpected and surprising behaviour of the anisotropic contribution to transverse relaxation, contradictory to the current understanding of the origins of relaxation anisotropy in ordered tissues. Type 2 diabetes mellitus is considered to be the ����epidemic of the 21st century���� and, consequently, the development of new therapies is one of the main challenges in drug discovery today. While current T2DM therapies that increase insulin secretion have proven to have beneficial therapeutic effects, these treatments often suffer from undesirable side effects such as hypoglycemia and weight gain. Therefore, there is a significant unmet medical need for better drugs to treat T2DM. Recently, the inhibition of human dipeptidyl peptidase-IV has emerged as a new treatment option for T2DM. This enzyme belongs to the serine protease family and selectively removes N-terminal dipeptides from substrates containing proline or alanine as the second residue. The most important substrates of BTB1 DPP-IV are incretins, such as glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. GLP-1 is released from intestinal L-cells in response to meals and performs the following actions: GLP-1 stimulates insulin biosynthesis and secretion, reduces glucagon release, slows gastric emptying, reduces appetite, and stimulates the regeneration and differentiation of islet B-cells. Alternatively, GIP is produced by the duodenal K-cells and is extensively involved in glucose metabolism by enhancing insulin secretion. Both peptides have very short half-lives because of their rapid degradation by DPP-IV. Inhibiting DPP-IV prolongs the action of GLP-1 and GIP, which, in turn, improves glucose homeostasis with a lower risk of hypoglycemia. Consequently, DPP-IV inhibitors are of considerable interest to the pharmaceutical industry, and intense research activities in this area have resulted in the launch of sitagliptin, saxagliptin, alogliptin, linagliptin and vildagliptin to the market. The DPP-IV Cyanopindolol hemifumarate binding site is highly druggable in the sense that tight and specific binding to the enzyme can be achieved with small molecules with drug-like physicochemical properties. The different interaction motifs used by these DPP-IV ligands include Ser630, the hydrophobic S1 pocket, the hydrophobic S2 pocket and the N-terminal recognition region.