Skip to main content
Log in

Topical Imiquimod

A Review of its Use in Genital Warts

  • Adis Drug Evaluation
  • Published:
Drugs Aims and scope Submit manuscript

Summary

Abstract

Imiquimod is a topically active immunomodulatory agent that is formulated as a 5% cream for application by the patient. It is the first agent of its class, the immune response modifiers, to be used in the treatment of genital warts. In immunocompetent patients with genital warts, imiquimod stimulates the production of interferon-α and various other cytokines, and has indirect antiviral activity.

In randomised, double-blind, vehicle-controlled clinical trials, complete clearance of warts occurred in 37 to 50% of immunocompetent patients with genital warts treated with imiquimod 5% cream 3 times a week for up to 16 weeks; partial clearance of warts (defined as a reduction in wart area of ≥50%) was observed in 76% of recipients of imiquimod 5% cream. Rates of complete orpartial clearance of warts were significantly higher in patients who applied imiquimod 5% cream 3 times a week than in recipients of imiquimod 1% or vehicle cream, each applied 3 times a week. A between-gender difference in clinical response to imiquimod 5% cream has been reported, with female patients experiencing higher rates of complete clearance of warts than males.

Recurrence(s) of ≥1 wart occurred in 13 to 19% of immunocompetent patients in whom complete clearance of warts had been achieved with imiquimod 5% cream.

Imiquimod 5% cream also shows some clearance of warts in immunosup-pressed HIV-infected patients with genital warts. Preliminary results of a vehicle-controlled study showed that the rate of partial clearance of warts (defined as a reduction in baseline wart area of >50%) [38%] was significantly higher with imiquimod 5% cream than with vehicle cream; however, the rate of complete clearance was not significantly higher than with vehicle cream.

Imiquimod 5% cream is generally well tolerated by immunocompetent and HIV-infected patients. Local skin reactions (mainly mild or moderate), including erythema, itching and burning, are the most commonly reported adverse events, occurring in ≤67% of patients applying imiquimod 5% cream 3 times a week. The incidence of adverse events is lower in patients applying the cream 3 times a week than with daily application. The incidence of systemic adverse events with imiquimod 5% cream (applied daily or 3 times a week) is similar to that of vehicle cream. The tolerability profile of imiquimod cream appears favourable compared with that of podophyllotoxin.

Conclusion: Imiquimod 5% cream is a new therapeutic option for patients with genital warts. It produces clearance rates broadly similar to those of other treatment approaches and rates of wart recurrence compare favourably with those reported for established treatments. In contrast to most alternative treatment strategies, which are administered in the physician’s office, imiquimod cream is a self-administered therapy for outpatient use.

Overview of Pharmacological Properties

Imiquimod, an imidazoquinoline, is a new type of treatment for genital warts. Its antiviral activity is mediated in part by its ability to stimulate the production of interferon-α and other cytokines. It is formulated as a 5% cream for application to genital warts by the patient.

In patients with genital warts receiving treatment with imiquimod 5% cream 3 times a week, a strong correlation between wart regression and increases in levels of mRNA for interferon-α, interferon-β, interferon-γ and tumour necrosis factor-α (TNF-α) in wart tissue has been observed. Increases in levels of mRNAs for interleukin (IL)-2 and 2′,5′-oligoadenylate synthetase (an effector protein induced by interferon) have also been reported.

Interferon-α, IL-6 and TNF-α production is stimulated by topical, oral or parenteral imiquimod in various animal models. The drug stimulates natural killer cell activity in mice and T cell activity in guinea pigs and mice. Exposure to imiquimod also leads to the proliferation and differentiation of B lymphocytes in vivo.

Imiquimod stimulates the production of some cytokines in human and animal monocyte/macrophage cells and in human keratinocytes in vitro. In human peripheral blood mononuclear cells (PBMCs), imiquimod induces the production of interferon-α, IL-1, IL-6, IL-8, IL-10, IL-12, TNF-α, granulocyte colony stimulating factor and granulocyte/macrophage colony-stimulating factor in vitro. Imiquimod increases expression of mRNAs for IL-6 and IL-8 but not mRNA for IL-1α in vitro in human keratinocytes and epidermal carcinoma cells. Levels of IL-8 have been shown to increase in human keratinocytes and fibroblast cultures exposed to imiquimod.

In patients with genital warts, imiquimod 5% cream applied 3 times a week significantly decreased levels of human papillomavirus (HPV) DNA and mRNA for the L1 HP gene in wart tissue, compared with baseline. Levels of HPV DNA and mRNA for the L1 HPV gene significantly correlated with wart regression.

Little information is available on the pharmacokinetics of imiquimod after application to the skin. In healthy volunteers, the drug shows minimal evidence of percutaneous absorption after topical application of a single 5mg dose.

Therapeutic Efficacy

The therapeutic efficacy of imiquimod cream (1 and 5% strengths) has been evaluated in 3 randomised, double-blind, vehicle-controlled trials that included 698 immunocompetent adults with genital warts. In these trials, imiquimod 5% cream was significantly more effective than imiquimod 1% cream or vehicle cream in achieving complete clearance of genital warts. Application of imiquimod 5% cream either daily or 3 times a week produced complete clearance of warts in 37 to 52% of patients (intention-to-treat data) in median times of 7 to 12 weeks; clearance rates were higher in the 2 trials of 16 weeks’ duration than in the trial of 8 weeks’ duration. Complete response rates in patients treated with imiquimod 1% cream were 14 and 21% and with vehicle cream ranged from 0 to 11%. Rates of complete clearance were higher in female than in male patients: 72 versus 33% in a trial of imiquimod applied 3 times a week and 64 versus 42% in another trial in which the cream was applied daily (intention-to-treat data).

Partial clearance of warts (defined as a reduction in baseline wart area of ≥50%) was documented after application of imiquimod 5% cream 3 times a week or daily for 16 weeks in 76 and 93% of patients.

Within a 12-week follow-up period, recurrence(s) of ≥1 wart(s) occurred in 13 to 19% of patients who had complete clearance with imiquimod 5% cream applied 3 times a week or daily. With 1% imiquimod cream applied 3 times a week or daily, recurrence rates were 17 and 0%.

Imiquimod 5% cream is also a beneficial treatment for some HIV-infected patients with genital warts, although response rates are lower than in immunocompetentindividuals. Preliminary results of a randomised, double-blind trial showed that complete clearance of warts occurred in 11 % of HIV-infected patients who applied imiquimod 5% cream 3 times a week for up to 16 weeks, compared with 6% of patients who applied the vehicle cream. Partial clearance of warts (defined as a reduction in wart area of >50%) occurred in significantly more recipients of imiquimod 5% cream than vehicle cream (38 vs 14%; p = 0.013).

Tolerability

Imiquimod 5% cream is generally well tolerated. Local skin reactions, including erythema, itching and burning, are the most common adverse events. These events are more common with daily application of imiquimod cream than with application 3 times a week. Local reactions occurred in significantly more recipients of imiquimod than vehicle cream (p < 0.05). Local erythema developed in 67% (71) patients who used imiquimod 5% cream; of these, 27.4, 34.0 and 5.7% had mild, moderate or severe symptoms. Rates of discontinuation of treatment because of adverse events ranged from 1 to 14% in clinical trials of imiquimod cream. The incidence of systemic adverse events, including headache and flu-like symptoms, with imiquimod 1 or 5% cream is similar to that with vehicle cream alone.

Dosage and Administration

Imiquimod is available as a 5% cream in single-use sachets. It is recommended that the cream is applied to cleaned and dried affected areas and washed off with soap and water 6 to 10 hours later. Imiquimod 5% cream should be applied 3 times a week either until the warts have cleared or for a maximum of 16 weeks.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Gangemi JD, Pirisi L, Angell M, et al. HPV replication in experimental models: effects of interferon. Antiviral Res 1994 Jul; 24: 175–90

    Article  PubMed  CAS  Google Scholar 

  2. Ferenczy A. Epidemiology and clinical pathophysiology of condylomata acuminata. Am J Obstet Gynecol 1995 Apr; 172 (Pt 2): 1331–9

    Article  PubMed  CAS  Google Scholar 

  3. Kraus SJ, Stone KM. Management of genital infection caused by human papillomavirus. Rev Infect Dis 1990 Jul–Aug; 12 Suppl. 6: S620–32

    Article  PubMed  Google Scholar 

  4. Oriel JD. Genitoanal papillomavirus infection — a diagnostic and therapeutic dilemma. Semin Dermatol 1990 Jun; 9: 141–7

    PubMed  CAS  Google Scholar 

  5. Richwald GA, Reitano M. New approaches to the management of external genital warts. Infect Dis Clin Pract 1999; 8: 67–75

    Article  Google Scholar 

  6. Stanley M. The immunology of genital human papilloma virus infection. Eur J Dermatol 1998 Oct–Nov; 8 Suppl. 7: 8–12

    PubMed  CAS  Google Scholar 

  7. Stanley MA, Masterson PJ, Nicholls PK. In vitro and animal models for antiviral therapy in papillomavirus infections. Antiviral Chem Chemother 1997 Sep; 8: 381–400

    CAS  Google Scholar 

  8. Majewski S, Jablonska S. Immunology of HPV infection and HPV-associated tumors. Int J Dermatol 1998 Feb; 37: 81–95

    Article  PubMed  CAS  Google Scholar 

  9. Stanley MA. Mini-review. Replication of human papillo-maviruses in cell culture. Antiviral Res 1994 May; 24: 1–15

    CAS  Google Scholar 

  10. Phillips TJ, Dover JS. Recent advances in dermatology. N Engl J Med 1992 Jan 16; 326: 167–78

    Article  PubMed  CAS  Google Scholar 

  11. Edwards L, Ferenczy A, Eron L, et al. Self-administered topical 5% imiquimod cream for external anogenital warts. Arch Dermatol 1998 Jan; 134: 25–30

    Article  PubMed  CAS  Google Scholar 

  12. Beutner KR, Spruance SL, Hougham AJ, et al. Treatment of genital warts with an immune-response modifier (imiquimod). J Am Acad Dermatol 1998 Feb; 38 (Pt 1): 230–9

    Article  PubMed  CAS  Google Scholar 

  13. Beutner KR, Geisse JK. Imiquimod — An immune-response modifier for the treatment of genital warts. Today’s Ther Trends 1997; 15(3): 165–78

    Google Scholar 

  14. Stone KM. Human papillomavirus infection and genital warts: update on epidemiology and treatment. Clin Infect Dis 1995 Apr; 20 Suppl. 1: 91–7

    Article  Google Scholar 

  15. Tindle RW, Frazer IH. Immunology of anogenital human papillomavirus (HPV) infection. Aust NZ J Obstet Gynaecol 1990 Nov; 30: 370–5

    Article  CAS  Google Scholar 

  16. Coleman N, Birley HDL, Renton AM, et al. Immunological events in regressing genital warts. Am J Clin Pathol 1994; 102: 768–74

    PubMed  CAS  Google Scholar 

  17. Czelusta AJ, Evans T, Arany I, et al. Aguide to immunotherapy of genital warts: focus on interferon and imiquimod. BioDrugs 1999; 11(5): 319–32

    Article  PubMed  CAS  Google Scholar 

  18. Reiter MJ, Testerman TL, Miller RL, et al. Cytokine induction in mice by the immunomodulator imiquimod. J Leukoc Biol 1994 Feb; 55: 234–40

    PubMed  CAS  Google Scholar 

  19. Slade HB. Cytokine induction and modifying the immune response to human papilloma virus with imiquimod. Eur J Dermatol 1998 Oct–Nov; 8 Suppl. 7: 13–6

    PubMed  CAS  Google Scholar 

  20. Miller R, Birmachu W, Gerster J, et al. Imiquimod: cytokine induction and antiviral activity. Int Antiviral News 1995 Aug; 3: 111–3

    Google Scholar 

  21. Miller RL, Gerster JF, Owens HB, et al. A review of imiquimod applied topically, a novel immune response modifier and new class of drug. 3M Pharmaceuticals, St Paul, Minnesota. Data on file, 1998

  22. Syed TA, Goswami J, Ahmadpour OA, et al. Treatment of molluscum contagiosum in males with an analog of imiquimod 1 % in cream: a placebo-controlled, double-blind study. J Dermatol 1998 May; 25: 309–13

    PubMed  CAS  Google Scholar 

  23. Syed TA, Ahmadpour OA, Ahmad SA. Treatment of genital herpes in males with imiquimod 1% cream: a randomised, double-blind, placebo-controlled study. Clin Drug Invest 1998 Sep; 16: 187–91

    Article  CAS  Google Scholar 

  24. Savage P, Horton V, Moore J, et al. A phase I clinical trial of imiquimod, an oral interferon inducer, administered daily. Br J Cancer 1996 Nov; 74: 1482–6

    Article  PubMed  CAS  Google Scholar 

  25. Goldstein D, Hertzog P, Tomkinson E, et al. Administration of imiquimod, an interferon inducer, in asymptomatic human immunodeficiency virus-infected persons to determine safety and biologic response modification. J Infect Dis 1998 Sep; 178: 858–61

    Article  PubMed  CAS  Google Scholar 

  26. Witt PL, Ritch PS, Reding D, et al. Phase I trial of an oral immunomodulator and interferon inducer in cancer patients. Cancer Res 1993 Nov 1; 53: 5176–80

    PubMed  CAS  Google Scholar 

  27. Tyring SK, Arany I, Stanley MA, et al. A randomized, controlled, molecular study of condylomata acuminata clearance during treatment with imiquimod. J Infect Dis 1998 Aug; 178: 551–5

    Article  PubMed  CAS  Google Scholar 

  28. Miller RL, Tomai MA, Arany I, et al. Cytokine induction in hairless mouse and human skin by topical immune response modifier, imiquimod [abstract]. J Invest Dermatol 1998 Apr; 110: 680

    Article  Google Scholar 

  29. Suzuki H, Wang B, Amerio P, et al. Topical immune response modifier imiquimod induces migration of Langerhans cells [abstract 010]. American Academy of Dermatology 57th Annual Meeting; 1999 Mar 19–24; New Orleans

  30. Bottrel RLA, Yang Y-L, Levy DE, et al. The immune response modifier imiquimod requires STAT-1 for induction of interferon, interferon-stimulated genes and interleukin-6. Anti-microb Agents Chemother 1999: 856–61

  31. Miller RL, Birmachu W, Gerster JF, et al. Cytokine induction by imiquimod: preclinical results and pharmacology. Chemotherapie Journal, Supplement 1995; 5(10): 52–4

    Google Scholar 

  32. Weeks CE, Gibson SJ. Induction of interferon and other cytokines by imiquimod and its hydroxylated metabolite R-842 in human blood cells in vitro. J Interferon Res 1994 Apr; 14: 81–5

    Article  PubMed  CAS  Google Scholar 

  33. Tomai M, Imbertson L, Wagner T, et al. Activation of human and mouse B lymphocytes by the immunomodulators imiquimod and S-27609 [abstract]. FASEB J 1994 Mar 15; 8: 253, Pt 1

    Google Scholar 

  34. Megyeri K, Rosztoczy I, Raj NBK, et al. Stimulation of interferon and cytokine gene expression by imiquimod: molecular mechanism. J Interferon Res 1994 Suppl. 5122

  35. Testerman TL, Gerster JF, Imbertson LM, et al. Cytokine induction by the immunomodulators imiquimod and S-27609. J Leukoc Biol 1995 Sep; 58: 365–72

    PubMed  CAS  Google Scholar 

  36. Gibson SJ, Imbertson LM, Wagner TL, et al. Cellular requirements for cytokine production in response to the immunomodulators imiquimod and S-27609. J Interferon Cytokine Res 1995 Jun; 15: 537–45

    Article  PubMed  CAS  Google Scholar 

  37. Megyeri K, Au W-C, Rosztoczy I, et al. Stimulation of interferon and cytokine gene expression by imiquimod and stimulation by Sendai virus utilize similar signal transduction pathways [published erratum appears in Mol Cell Biol 1995 May; 15 (5): 2905]. Mol Cell Biol 1995 Apr; 15: 2207–18

    PubMed  CAS  Google Scholar 

  38. Wagner TL, Horton VL, Carlson GL, et al. Induction of cytokines in cynomolgus monkeys by the immune response modifiers, imiquimod, S-27609 and S-28463. Cytokine 1997 Nov; 9: 837–45

    Article  PubMed  CAS  Google Scholar 

  39. Wagner TL, Ahonen CL, Couture AM, et al. Modulation of TH1 and TH2 cytokine production with the immune response modifiers, R-848 and imiquimod. Cell Immunol 1999; 191: 10–9

    Article  PubMed  CAS  Google Scholar 

  40. Burns R, Tomai MA, Miller RL, et al. The imidazoquinolines, imiquimod (R837) and R-848 both induce functional but not phenotypic maturation of human epidermal Langerhans cells in vitro [abstract 281]. American Academy of Dermatology 57th Annual Meeting; 1999 Mar 19–24; New Orleans

  41. Burns R, Ferbel B, Tomai MA, et al. The imidazoquinilones, imiquimod (R-837) and R-842 both induce functional but not phenotypic maturation of human epidermal Langerhans cells in vitro [abstract). J Invest Dermatol 1999; 112(4): 534

    Google Scholar 

  42. Kono T, Kondo S, Pastore S, et al. Effects of a novel topical immunomodulator, imiquimod, on keratinocyte cytokine gene expression. Lymphokine Cytokine Res 1994 Apr; 13: 71–6

    PubMed  CAS  Google Scholar 

  43. Imbertson LM, Beaurline JM, Couture AM, et al. Cytokine induction in hairless mouse and rat skin after topical application of the immune response modifiers imiquimod and S-28463. J Invest Dermatol 1998 May; 110: 734–9

    Article  PubMed  CAS  Google Scholar 

  44. Tomai MA, Birmachu W, Case MT, et al. Imiquimod: in vivo and in vitro characteristics and toxicology. In: Aly R, Beutner KR, Maibach HI, editors. Cutaneous infection and therapy. Vol. 32. New York: Dekker, 1997

    Google Scholar 

  45. Miller RL, Tomai MA, Ahonen CL, et al. Effects of the imidazoquinolines, imiquimod and S-28463, on TH1 and TH2 cytokine responses in vitro [abstract 280]. American Academy of Dermatology 57th Annual Meeting; 1999 Mar 19–24; New Orleans

  46. McDermott DJ, Senta TA, Smith MH, et al. Arising single dose safety, pharmacokinetic and pharmacodynamic study of imiquimod (Aldara™) applied to the cervix of healthy female volunteers [poster]. 17th International Papillomavirus Conference. 1999 Jan 5–15; Charleston

  47. Tomai MA, Gibson SJ, Imbertson LM, et al. Immunomodulating and antiviral activities of the imidazoquinoline S-28463. Antiviral Res 1995; 28: 253–64

    Article  PubMed  CAS  Google Scholar 

  48. Tomai MA, Gibson SJ, Gerster JF, et al. Immunomodulating activities of imiquimod, and its analogs, S-27609 and S-28463 in human keratinocyte and fibroblast cultures and mouse skin [abstract]. J Invest Dermatol 1995 Apr; 104: 692

    Google Scholar 

  49. Fujisawa H, Shivji GM, Kondo S, et al. Effect of a novel topical immunomodulator, S-28463, on keratinocyte cytokine gene expression and production. J Interferon Cytokine Res 1996 Jul; 16: 555–9

    Article  PubMed  CAS  Google Scholar 

  50. Tomai MA, Gibson SJ, Imbertson LM, et al. Immunomodulating and antiviral activities of the imidazoquinoline S-28463. Antiviral Res 1995 Nov; 28: 253–64

    Article  PubMed  CAS  Google Scholar 

  51. Owens ML, Tygum KI, Senta TA, et al. A safety assessment of topical imiquimod [abstract]. 19th World Congress of Dermatology; 1997 Jun 15–20, Sydney

  52. Tygum KI, Smith SL, Myers JA, et al. Percutaneous penetration of [14C]imiquimod from a single application of cream [abstract]. Pharm Res 1995 Sep; 12 Suppl.: 277

    Google Scholar 

  53. Beutner KR, Tyring SK, Trofatter Jr JKF, et al. Imiquimod, a patient-applied immune-response modifier for treatment of external genital warts. Antimicrob Agents Chemother 1998 Apr; 42: 789–94

    PubMed  CAS  Google Scholar 

  54. Conant MA, Opp KM, Gilson RJC, et al. A vehicle-controlled safety and efficacy trial evaluating 5% imiquimod cream for the treatment of genital/perianal warts in HIV-positive patients [abstract]. American Academy of Dermatology 56th Annual Meeting; 1998 Feb 27–March 4, Orlando (FL)

  55. Trofatter Jr JKF. Imiquimod in clinical practice. Eur J Dermatol 1998 Oct–Nov; 8 Suppl. 7: 17–9

    PubMed  CAS  Google Scholar 

  56. 3M launches Aldara in the UK. Scrip 1998 Oct 7 (2376): 19

  57. Imiquimod cream for genital warts. Am Fam Physician 1997; 55(6): 2348

    Google Scholar 

  58. US Department of Health and Human Services. 1998 Guidelines for treatment of sexually transmitted diseases. MMWR Morb Mortal Wkly Rep 1998; 47 (RR-1)

  59. Maw RD, Reitano M, Roy M. An international survey of patients with genital warts: perceptions regarding treatment and impact on lifestyle. Int J STD AIDS 1998; 9: 571–8

    Article  PubMed  CAS  Google Scholar 

  60. Beutner KR, Wiley DJ, Douglas JM, et al. Genital warts and their treatment. Clin Infect Dis 1998; 28 Suppl. 1: S37–56

    Article  Google Scholar 

  61. Beutner KR, Ferenczy A. Therapeutic approaches to genital warts. Am J Med 1997 May 5; 102 Suppl. 5A: 28–37

    Article  PubMed  CAS  Google Scholar 

  62. Cowsert LM. Treatment of papillomavirus infections: recent practice and future approaches. Intervirology 1994 May–Aug; 37: 226–30

    PubMed  CAS  Google Scholar 

  63. Mayeaux JR EJ, Spigener SD. Treatment of human genital papillomavirus infections. Hosp Pract 1997; 32(12): 87–90

    Google Scholar 

  64. Marcus J, Camisa C. Podophyllin therapy for condyloma acuminatum. Int J Dermatol 1990 Dec; 29: 693–8

    Article  PubMed  CAS  Google Scholar 

  65. Langley PC, Tyring SK, Smith MH. The cost-effectiveness of patient-applied versus provider-administered intervention strategies for the treatment of external genital warts. Am J Managed Care 1999; 5(1): 69–77

    CAS  Google Scholar 

  66. Lebwohl M, Contard P. Interferon and condylomata acuminata. Int J Dermatol 1990 Dec; 29: 699–705

    Article  PubMed  CAS  Google Scholar 

  67. Cirelli R, Tyring SK. Interferons in human papillomavirus infections. Antiviral Res 1994 Jul; 24: 191–204

    Article  PubMed  CAS  Google Scholar 

  68. Stuart-Harris RC, Lauchlan R, Day R, et al. The clinical application of the interferons: a review. Med J Aust 1992 Jun 15; 156: 869–72

    PubMed  CAS  Google Scholar 

  69. Fife KH. New treatments for genital warts less than ideal: abstract and commentary. JAMA 1998 Jun 24; 279: 2003–4

    Article  PubMed  CAS  Google Scholar 

  70. Tyring S, Edwards L, Cherry LK, et al. Safety and efficacy of 0.5% podofilox gel in the treatment of anogenital warts. Arch Dermatol 1998; 134: 33–8

    Article  PubMed  CAS  Google Scholar 

  71. Petersen CS, Weismann K. Quercetin and kaempherol: an argument against the use of podophyllin? Genitourin Med 1995; 71: 92–3

    PubMed  CAS  Google Scholar 

  72. Greenberg MD, Rutledge LH, Reid R, et al. A double-blind, randomized trial of 0.5% podofilox and placebo for the treatment of genital warts in women. Obstet Gynecol 1991; 77: 735–9

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Caroline M. Perry.

Additional information

Various sections of the manuscript reviewed by: P.L. Anderson, Department of Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, Minnesota, USA; K.R. Beutner, Solano Dermatology Associates, Vallejo, California, USA; K.H. Fife, Indiana University School of Medicine, Indianapolis, Indiana, USA; C.V. Fletcher, Department of Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, Minnesota, USA; B.G. Gazzard, Chelsea and Westminster Healthcare National Health Service Trust, Chelsea and Westminster Hospital, London, England; M.A. Stanley, Department of Pathology, Division of Cellular Pathology, University of Cambridge, Cambridge, England; S.K. Tyring, The University of Texas Medical Branch Center for Clinical Studies, University of Texas, Houston, Texas, USA.

Data Selection

Sources: Medical literature published in any language since 1966 on Imiquimod, identified using AdisBase (a proprietary database of Adis International, Auckland, New Zealand), Medline and EMBASE. Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.

Search strategy: AdisBase search terms were ‘Imiquimod’ or ‘DZ-2636’ or ‘R-837’ or ‘S-26308’. Medline search terms were ‘Imiquimod’ or ‘R-837’ or ‘S-26308’. EMBASE search terms were ‘Imiquimod’ or ‘R-837’ or ‘S-26308’. Searches were last updated on 14 July 1999.

Selection: Studies in patients with genital warts who received treatment with imiquimod. Inclusion of studies was based mainly on the methods section of the trials. When available, large, well controlled trials with appropriate statistical methodology were preferred. Relevant pharmacodynamic and pharmacokinetic data are also included.

Index terms: Imiquimod, pharmacodynamics, pharmacokinetics, therapeutic use.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Perry, C.M., Lamb, H.M. Topical Imiquimod. Drugs 58, 375–390 (1999). https://doi.org/10.2165/00003495-199958020-00017

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.2165/00003495-199958020-00017

Keywords

Navigation