# Soriasis: From Pathogenesis to Pharmacological and Nano-Technological-Based Therapeutics
## 3 Current Marketed Therapies
\begin{table}
\begin{tabular}{c c c c} \hline
**Type of** & **Effects** & **Drawbacks** & **References** \\ \hline \multirow{6}{*}{Acitretin} & & & Depression, \\  & & It binds to nuclear receptors on genes & hypertriglyceridemia and \\  & & controlling cellular differentiation, & hypercholesterolemia, \\  & & anti-proliferation, anti-inflammation, & Mylagias, cheilitis, skin \\  & & anti-keratinization, and inhibition of & peeling, alopecia, xerosis, \\  & & neutrophil chemotaxis. It is the only systemic & rhinitis, nail dystrophy, \\  & & treatment that is not immunosuppressive. & epistaxis, sticky skin, retinoid \\  & & dermatitis, and xerophthalmia. & \\ \hline \multirow{6}{*}{Conventional treatments} & & & Warmth, reddening of the face, \\  & & It has immunomoddulatory, anti-inflammatory, & and and headaches, proteinuria, \\  & Esthers (FAEs) & and antiproliferative properties and apoptotic & reversible renal insufficiency, \\  & & actions on activated T cells. & microscopic haematuria, and \\  & & & proximal tubular damage. \\ \hline \multirow{6}{*}{Cyclosporine} & & & Hypertension, arrhythmia, \\  & & It inhibits Interleukin synthesis, such as IL-2 & hypertension, anxiety, \\  & & and T cell differentiation. & headaches, fever, \\  & & & hypomagnesemia, \\  & & & hyperkalaemia, dyslipidemia, \\  & & and encephalopathy. & \\ \hline \multirow{6}{*}{Methodrexate} & & It reduces interleukin (IL)-17 mRNA and & \\  & & IL-17 protein expression in CD3- and & \\  & & CD28-stimulated peripheral blood & \\  & & mononuclear cells. It modulates & \\  & & pro-inflammatory mediators and its effects on & \\  & & atherogenic gene expression in psoriatic & \\  & & lesion skin. & \\ \hline \multirow{6}{*}{Small molecules} & & It inhibits the expression and/or & \\  & & production of TNF-\(\alpha\), IFN- \(c\), IL-12, and IL-23 & \\  & & and the chemokines CXCL9, CXCL10, CCL2, & \\  & & and CCL3, IL-2, IL-5, IL-13, IL-17, TNF-\(\alpha\), and & \\  & & IFN-c by stimulated T cells and IFN-a by & \\  & & dendritic cells. & \\ \hline \multirow{6}{*}{Small molecules} & & It is a potent inhibitor of JAK1 and JAK3 and & Nasopharyngealsitis, upper \\  & & has some activity against JAK2 and Tyk2. & respiratory tract infection, \\ \cline{1-1}  & & & headache, urinary tract \\ \cline{1-1}  & & infection, and diarrhoea. & \\ \hline \hline \end{tabular}
\end{table} 
Table 2: Accepted systemic treatments. \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Type of Treatment** & **Drug** & **Effects** & **Drawbacks** & **References** \\ \hline \multirow{8}{*}{Anti-TNF alpha} & \multirow{3}{*}{Infiximab} & It interferes with the actions of TNF-\(\alpha\) & \multirow{3}{*}{Dyspnoea, urticaria, hypotension, flushing, and headache.} & \multirow{3}{*}{[83]} \\  & & by directly binding to soluble and & \\  & & transmembrane TNF-\(\alpha\) molecules in the & & \\  & & plasma and the diseased tissue. & & \\ \cline{2-5}  & \multirow{4}{*}{Etancercept} & It is a recombinant human TNF-recipient by & \multirow{4}{*}{Respiratory infections, flu-like symptoms, and } \\  & & Not fusion protein that antagonizes the effects & & \\  & & of endogenous TNF by competitively & & \\  & & inhibiting its in- & & \\  & & study disintegration with cell-surface & & \\  & & receptors. & & \\ \hline \multirow{8}{*}{Anti-TNF alpha} & \multirow{3}{*}{Etancercept} & It blocks its interaction with the p55 and p75 & Headache, nausea, elevated triglycerides, cough, sinus congestion, and fatigue most common. & \multirow{3}{*}{[86]} \\  & & cell surface TNF receptors. & & \\  & & common. & & \\ \cline{2-5}  & \multirow{4}{*}{Certolizumab} & It inhibits lipopolysaccharide-induced IL-1-\(\beta\) & Headache, nasopharyngitis, upper respiratory tract infections, diarrhoea, and & \\  & & \(\alpha\)-expressing cells.