## 1 Introduction
Dithranol itself is derived from chrysarobin [29]; therefore, it is not surprising that some efforts have been directed towards the improvement of the therapeutic index of dithranol by attempting to separate the beneficial effects from the side effects of the drug. This has been realized by the development of new derivates [30; 31; 32; 33], where the staining effect of the drug would be at least theoretically reduced (Figure 3). The ability of dithranol to induce keratinocyte differentiation was investigated and correlated with its potency to inhibit the proliferation of keratinocytes [34; 35]. To determine the structural requirements for this effect, dithranol and 17 analogues or related anthracones were examined for their ability to induce the formation of the cornified envelope (a marker of terminal differentiation). Moreover, dithranol, dithranol dimer, and dithranol triacetate exhibited antiproliferative and antirespiratory activity at concentrations required to induce keratinocyte differentiation, suggesting causality between these effects. In addition, cornified envelope formation was observed for several related anthracones at low concentrations. In general, compounds containing benzoyl substituents, independent of their position in the anthralin nucleus, were more potent than those with benzyl substituents. The basic principles include combined treatment. The idea is to increase the efficiency and decrease the adverse effects of the treatment. This combination of drugs is not accidental but arises from pathogenesis diseases, where it is necessary to  
Figure 3: Chemical modifications of dithranol, proposed as a possible new antisporiatic drug. Figure 2: Chemical structures of main degradation products of dithranol: danthron (1.8-dihydroxyarthracene-9,10-dione) and bianthrone (4,4\({}^{\prime}\),5,5\({}^{\prime}\)-tetrahydrooxy-[9,9\({}^{\prime}\)-bianthracene]-10,10\({}^{\prime}\)(9H,9\({}^{\prime}\)H)-dione). suppress both immunopathological inflammation and, on the other hand, a disorder of differentiation and apoptosis. In most therapeutic regimes, dithranol is combined with salicylic acid [17; 28]. Salicylic acid is an important ingredient in many skin products that treat acne, psoriasis, corns, keratosis pirlaris, and warts, utilizing its keratolytic, analgesic, antibacterial, and anti-inflammatory properties [36]. It is advantageous if combination therapy can be administered in the form of a prodrug, where two drugs working against the same condition are joined by a cleavable covalent bond. Examples of prodrugs based on the enzymatic hydrolysis of ester bond-activated drug release are rather common, e.g., procaine, simvastatin, and enalapril [37; 38]. The dithranol hydroxyl -OH moiety and the complementary carboxylic group -COOH group of salicylic acid (SAL) are optimal sites of ester bonds for synthesizing the prodrug DIT-SAL, comprising dithranol and salicylic acid in a 1:1 stoichiometric ratio (Figure 4). Such a conjugation of DIT and SAL can lead to better skin absorption than for original drugs, as has been demonstrated, e.g., for a naproxen-dithranol antiposoriatic prodrug [39; 40], as well as for a hydroquinone-salicylic acid prodrug [41] for the treatment of melanoma. The aim of this work is to find the molecular structure, vibrational spectra, molecular orbitals, MEP (molecular electric potential), UV-VIS spectra, TDOS (total density of states), RDG (reduced density gradient) analysis, and ADME in silico modelling of the DIT-SAL molecule by using reliable computational methods of quantum chemistry.