Footmender All In One Foot Cream has eight active ingredients that create the following effects: antimicrobial effect that prevents the regrowth of microorganisms for at least 12 hours; an exfoliating effect that removes dead skin cells; footmender binds and retains moisture in the skin; softens the skin; reduces skin sensitivity and slows the release of water; stabilises skin cell renewal; stimulates the healing of cracked skin and strengthens the skin’s barrier effect

Delgocitinib is a pan Janus kinase (JAK) inhibitor that targets the activity of all four members of the JAK family of enzymes consisting of JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2) in a concentration dependent manner.

The active ingredients in Enstilar Cutaneous Foam are calcipotriol (as monohydrate) and betamethasone (as dipropionate). Enstilar contains a combination of calcipotriol and betamethasone dipropionate. Calcipotriol is a vitamin D analogue. In vitro data suggest that calcipotriol induces differentiation and suppresses proliferation of keratinocytes. This is the proposed basis for its effect in psoriasis. Betamethasone dipropionate is a potent topical corticosteroid with anti-inflammatory, antipruritic, vasoconstrictive and immunosuppressive properties, although it does not cure the underlying condition.

Calcipotriol is a vitamin D derivative. In vitro data suggest that it induces differentiation and suppresses proliferation of keratinocytes. This is the proposed basis for its effect in psoriasis

Contains calcipotriol and betamethasone. Calcipotriol helps to bring the rate of skin cell growth back to normal and betamethasone acts to reduce inflammation.

Brodalumab is a recombinant fully human monoclonal immunoglobulin IgG2 antibody that binds with high affinity to human IL-17RA and blocks the biological activities of the pro-inflammatory cytokines IL-17A, IL-17F, IL-17A/F heterodimer and IL-25, resulting in inhibition of the inflammation and clinical symptoms associated with psoriasis. IL-17RA is a protein expressed on the cell surface and is a required component of receptor complexes used by multiple IL-17 family cytokines. IL-17 family cytokine concentrations have been reported to be increased in psoriasis. Blocking IL-17RA inhibits IL-17 cytokine-induced responses resulting in normalisation of inflammation in the skin.

Fucibet Lipid Cream combines the well-known anti-inflammatory and antipruritic effects of betamethasone with the topical antibacterial action of fusidic acid. Betamethasone valerate is a topical steroid that is rapidly effective in inflammatory dermatoses that normally respond to this form of therapy. More refractory conditions can often be treated successfully. When applied topically, fusidic acid is effective against Staphylococcus aureus, Streptococcus, Corynebacterium, Neisseria and certain clostridia and Bacteroides. Concentrations of 0.03-0.12µ per ml inhibit nearly all strains of S. aureus. The antibacterial activity of fusidic acid is not diminished in the presence of betamethasone

Fucibet Cream combines the well-known anti-inflammatory and antipruritic effects of betamethasone with the topical antibacterial action of fusidic acid. Betamethasone valerate is a topical steroid that is rapidly effective in inflammatory dermatoses that normally respond to this form of therapy. More refractory conditions can often be treated successfully. When applied topically, fusidic acid is effective against Staphylococcus aureus, Streptococcus, Corynebacterium, Neisseria and certain clostridia and Bacteroides. Concentrations of 0.03-0.12µg per ml inhibit nearly all strains of S. aureus. The antibacterial activity of fusidic acid is not diminished in the presence of betamethasone

Fucidin H Cream combines the potent topical antibacterial action of fusidic acid with the anti-inflammatory and antipruritic effects of hydrocortisone. Concentrations of 0.03–0.12µg/ml of fusidic acid inhibit nearly all strains of Staphylococcus aureus. Topical application of fusidic acid is also effective against Streptococcus, Corynebacterium, Neisseria and certain clostridia

The mechanism of action of tacrolimus in atopic dermatitis is not fully understood. Whilethe following have been observed, the clinical significance of these observations in atopicdermatitis is not known. Via its binding to a specific cytoplasmic immunophilin (FKBP12),tacrolimus inhibits calcium-dependent signal transduction pathways in T cells, therebypreventing the transcription and synthesis of IL-2, IL-3, IL-4, IL-5 and other cytokines such asGM-CSF, TNF-α and IFN-γ. In patients with atopic dermatitis, improvement of skin lesionsduring treatment with tacrolimus ointment was associated with reduced Fc receptorexpression on Langerhans cells and a reduction of their hyperstimulatory activity towards Tcells. Tacrolimus ointment does not affect collagen synthesis in humans.