## 1 Introduction  
Sporiasis is a multifactorial immune-mediated systemic disease with a number of comorbidities [1, 2, 3, 4, 5, 6, 7, 8]. The exact cause of psoriasis, which affects about 150 million people worldwide, is not fully understood. The genetic component plays an important role. Its heredity component is polygenic or multifactorial. The disposition to the disease (posoriatic dithensis, latent psoriasis) is inherited, not the disease itself. Due to its relatively high prevalence in the population, its chronic course, and the significant percentage of severe forms, it is one of the most pharmacoeconomically demanding diseases. The key features of psoriasis are  
1. Red patches: the affected areas of the skin are red and inflamed. 2. Silvery scales: overlying the red patches, there are often silvery or white scales. 3. Itching and discomfort: psoriasis plaques can be itchy, and the skin may feel sore or painful. 4. Nail changes: psoriasis can also affect the nails, causing changes such as pitting, discoloration, and separation from the nail bed. Psoriasis therapeutic modes include:  
1. Topical treatments: these include corticosteroid creams, vitamin D analogues, retinoids, dithranol, coal tar, and moisturizers. 2. Phototherapy: exposure to ultraviolet light can be beneficial for some individuals with psoriasis. 3. Systemic medications: In cases of moderate-to-severe psoriasis, oral or injectable medications (e.g., methotrexate) can be used. 4. Biologics: these are a newer class of medications that target specific components of the immune system involved in the development of psoriasis (e.g., IL 12/23 blocker-ustkeinumab and anti-IL-17-secukinumab). The development of effective local treatments involves not only the discovery of new therapeutic substances but also advancements in the formulation or preparation of these substances [9; 10; 11]. One of the most successful drugs used in treatment of psoriasis is dithranol (Figure 1), also called anthralin [12; 13; 14; 15; 16; 17; 18; 19], routinely used since 1916 [18], but the antiposoriatic effect of chrysarobin, the precursor of dithranol, a substance of plant origin, was described as early as 1876 by [PERSON]. Dithranol (DIT) inhibits the synthesis of DNA that hyperprolifates the epidermis, adjusts the cycle of epidermal renewal, suppresses the production of products of the arachidonic acid cascade, suppresses the penetration of neutrophils into the epidermis, limits the activation of lymphocytes and the function of dendritic cells in target cells, acts at the level of mitochondria, and thus has several desired effects precisely in the psoriatic process [20]. The combination of dithranol with sub-erythemal doses of UVB (an amount of UVB that is insufficient to cause erythema-skin reddening, which is a measure of the amount of UVB that penetrates the skin without causing any visible damage) is the principle of the so-called Ingram treatment. The manifestations are freed of scales, irradiated with a UVB lamp, and then accurately treated with dithranol in a trap or ointment. Its initial concentration is 0.1%, with a gradual increase in concentration to 4 percent if the skin's reaction allows. This procedure is repeated after 18 to 22 h. Most patients recover within 3 weeks [21; 22]. Unpleasant brown-violet coloration [23] and skin irritation due to the formation of dithranol metabolites such as danthron and bianthrone (Figure 2) at the application site formed upon the exposure of dithranol to atmospheric oxygen are the main reasons for its limited usage [24; 25; 26; 27; 28]. It cannot be applied to the area of the head and neck, the bends of large joints, or the external genitalia. Figure 1: Chemical structures of dithranol (1,8-dihydroxyanthracen-9(10H)-one) and chrysarobin (1,8-dihydroxy-3-methylanthracen-9(10H)-one).