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Antiviral Treatment
Published in Marie Studahl, Paola Cinque, Tomas Bergström, Herpes Simplex Viruses, 2017
In clinical trials are resiquimod (S-28463, R-848), A-5021 (AV-038), SP-303 (Virend®), a vaccine (see Chap. 2) and soon helicase primase inhibitors. A topical formulation (0.5%) of resiquimod (Fig. 1) has been developed as an immunomodulator of HSV infections. Phase III clinical trials were terminated due to lack of efficacy. Imidazoquinolines bind to cell surface receptors, such as Toll receptor 7, thereby inducing secretion of proinflammatory cyokines, predominantly inferferon-alpha, tumor necrosis factor-alpha, and interleukin-12. This locally generated cytokine milieu biases towards a Th1 cell-mediated immune response with generation of cytotoxic effectors. The immunostimulatory effects have been exploited clinically in treatment of viral infections (HPV, HSV, and mooluscum contagiosum) and nonmela-noma skin cancer.
Resiquimod: a new topical immune-response modifier for the treatment of actinic keratosis
Published in Expert Opinion on Emerging Drugs, 2021
Morgan A. Farr, Tejas P. Joshi, Daniel J. Lewis
We read with great interest the review article by Cramer and Stockfleth, which highlights novel therapies for actinic keratosis (AK) [1]. In particular, the authors note imiquimod to be of therapeutic value in AK. Resiquimod is an emerging therapy that too should be considered part of the therapeutic armamentarium against AK. Like imiquimod, resiquimod belongs to the class of imidazoquinolines, small organic molecules with potent antiviral and anticancer activity. Resiquimod is a Toll-like receptor (TLR)-7 and TLR-8 agonist that activates myeloid and plasmacytoid dendritic cells. In addition, resiquimod may promote the release of cytokines – interleukin-6, tumor necrosis factor-α, and interferon-α – more effectively than imiquimod. Therefore, resiquimod may achieve greater efficacy than imiquimod based on its pharmacodynamic profile and thus is emerging as a new topical pharmacotherapy for AK [2].
Trial Watch: experimental TLR7/TLR8 agonists for oncological indications
Published in OncoImmunology, 2020
Giorgio Frega, Qi Wu, Julie Le Naour, Erika Vacchelli, Lorenzo Galluzzi, Guido Kroemer, Oliver Kepp
Topical resiquimod has been tested as a standalone therapeutic intervention in 217 patients with actinic keratosis, a common precancerous lesion of the skin that is linked to excessive sun exposure,78,99,100 with the purpose of determining optimal dose with respect to efficacy, safety and tolerability (NCT01583816).92 Patients were randomize to daily 0.01% or 0.03% resiquimod cream in five different treatment schedules until skin erosion or up to 8 weeks. Complete clinical clearance was obtained in up 56% to 85% of patients, depending on study group, with maximal efficacy being observed among individual receiving the 0.03% formulation.92 One hundred and twenty-eight patients experience treatment-related adverse effects (TRAEs), the majority of which was mild.92
Emerging drugs for the treatment of basal cell carcinoma
Published in Expert Opinion on Emerging Drugs, 2021
Florian Herms, Nicole Basset-Seguin
Unlike imiquimod, resiquimod is an immune response modifier (TLR 7 and TLR8 agonist), which may induce greater responses than imiquimod [45]. Its activity against actinic keratosis has been demonstrated in a phase 2 study (NCT01583816) [46]. A phase 1/2 study evaluating the safety and efficacy of resiquimod gel 0.06% for patients with nBCC is ongoing (NCT01808950). Resiquimod will be applied once daily, 5 times a week for 4 weeks. Three different arms of treatment are evaluated: 60 mg or 100 mg on nBCC, and 100 mg after shaving of nBCC.