PSUMMIT I studied the PsA patient na?ve to TNF brokers and, practically, many PsA patients are treated with these brokers. the three major trials conducted to show the efficacy and security of UST in PsA. 2007]. In September 2009, the US Food and Drug Administration (FDA) approved its use for adult patients with moderate-to-severe plaque psoriasis. It has also been approved in Canada and Europe to treat moderate-to-severe plaque psoriasis. Like psoriasis, psoriatic arthritis (PsA) is an important systemic inflammatory disorder characterized by the association of inflammatory arthritis with skin psoriasis. Tumor necrosis factor (TNF) inhibitors have proven highly effective for PsA, with significant improvements in articular and dermatologic involvement, enhanced quality of life and functional status, and inhibition of radiographic joint damage [Antoni 2005; Gladman, 2002; Mease 2004, 2005]. However, not all PsA patients respond to TNF inhibitor therapy, highlighting the need for additional treatment modalities with unique mechanisms of action. Also, many patients stop responding to these brokers after a certain period of use. A significant number of patients have a recurrent course or a prolonged disease process. To meet these challenges, a new agent working on different inflammatory aspect of PsA is needed. Until recently, the exact role of UST in the management of PsA had not been very clear. This short article reviews the mechanism of (S,R,S)-AHPC-PEG3-NH2 action, pharmacokinetics, efficacy, security profile and the clinical potential of UST in patients with PsA. Mechanism of action of ustekinumab in PsA Like psoriasis, acquired immunity involving the Th17/IL-23 axis is considered to play an important role in PsA [Di Cesare 2009; Lowes 2008]. However, differences have been suggested between arthritis-specific pathology and cutaneous psoriatic lesions. genes, psoriasis and PsA Cargill and colleagues have shown that psoriasis susceptibility is usually associated with single-nucleotide polymorphisms (SNPs) within the interleukin-23 receptor (IL-23R) and IL-12B, the gene that encodes for subunit of ligand of IL-23R [Cargill 2008]. Given the active involvement of IL-12 and IL-23 in the pathogenesis of psoriasis and genetic susceptibility with SNPs within IL-23R and IL-12B, it will be interesting to know if comparable exist for PsA. Recently, it was shown that PsA-like psoriasis is usually associated with variance in both of the above genes [Filer 2008]. The effect sizes seen were smaller with PsA GDF5 than psoriasis but were statistically significant [Filer 2008]. Since, the criteria for enrolling PsA patients in this article was to obtain the DNA samples from your patients with psoriasis and inflammatory arthritis, concluding association of genes solely with PsA would be impossible. IL-12 and IL-23 are essential for the induction and maintenance of the Th1/Th17 immune response, respectively, which is the main cytokine profile of psoriasis [Di Cesare 2009; Lowes 2008]. IL-23 activates Th17, which produces interleukin-17 (IL-17), activating dendritic cells to produce IL-12, hence stimulating Th1 [Di Cesare 2009; Lowes 2008]. Comparable involvement of IL-12 and IL-23 in the pathogenesis and comparable susceptibility loci might predispose one to think that a drug affecting these should produce similar results in psoriasis and PsA. Given the frequent association of both entities, it is difficult (S,R,S)-AHPC-PEG3-NH2 to conclude any true relation. We discuss the clinical potential of UST in the management of PsA later in the article. Pharmacokinetics Zhu and colleagues analyzed the data from phase II trials of UST in patients with PsA to characterize the population pharmacokinetics of subcutaneous UST and compared them with those from patients with moderate-to-severe plaque psoriasis [Zhu 2010]. They concluded that the pharmacokinetics of UST in patients with PsA is comparable with that of patients with moderate-to-severe plaque psoriasis in terms of population typical imply values for apparent clearance (CL/F), apparent volume of distribution (V/F) and absorption rate constant. Apart from the body weight and antibody status of patients, none of the other factors including previous (S,R,S)-AHPC-PEG3-NH2 treatment modalities were responsible for intersubject variability in CL/F and/or V/F. The comparable pharmacokinetics in PsA patients further strengthens the fact that UST should produce similar results in both psoriasis and PsA [Zhu 2010]. Although, such hypothesis would need more proof and we will discuss in details below.