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Also known as: 99011-02-6, Aldara, Zyclara, 1-isobutyl-1h-imidazo[4,5-c]quinolin-4-amine, 1-(2-methylpropyl)-1h-imidazo[4,5-c]quinolin-4-amine, Beselna
Molecular Formula
C14H16N4
Molecular Weight
240.30  g/mol
InChI Key
DOUYETYNHWVLEO-UHFFFAOYSA-N
FDA UNII
P1QW714R7M

Imiquimod
A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS.
The mechanism of action of imiquimod is as an Interferon Inducer. The physiologic effect of imiquimod is by means of Increased Cytokine Activity, and Increased Cytokine Production.
1 2D Structure

Imiquimod

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
1-(2-methylpropyl)imidazo[4,5-c]quinolin-4-amine
2.1.2 InChI
InChI=1S/C14H16N4/c1-9(2)7-18-8-16-12-13(18)10-5-3-4-6-11(10)17-14(12)15/h3-6,8-9H,7H2,1-2H3,(H2,15,17)
2.1.3 InChI Key
DOUYETYNHWVLEO-UHFFFAOYSA-N
2.1.4 Canonical SMILES
CC(C)CN1C=NC2=C1C3=CC=CC=C3N=C2N
2.2 Other Identifiers
2.2.1 UNII
P1QW714R7M
2.3 Synonyms
2.3.1 MeSH Synonyms

1. 1-isobutyl-1h-imidazo(4,5-c)quinolin-4-amine

2. Aldara

3. R 837

4. R-837

5. R837

6. S 26308

7. S-26308

8. Zyclara

2.3.2 Depositor-Supplied Synonyms

1. 99011-02-6

2. Aldara

3. Zyclara

4. 1-isobutyl-1h-imidazo[4,5-c]quinolin-4-amine

5. 1-(2-methylpropyl)-1h-imidazo[4,5-c]quinolin-4-amine

6. Beselna

7. 4-amino-1-isobutyl-1h-imidazo[4,5-c]quinoline

8. R 837

9. 1-(2-methylpropyl)imidazo[4,5-c]quinolin-4-amine

10. 4-amino-1-isobutyl-1h-imidazo(4,5-c)quinoline

11. 9050-31-1

12. R-837

13. S-26308

14. C14h16n4

15. Mfcd00866946

16. Tmx-101

17. S26308

18. Nsc-369100

19. Nsc-759651

20. Chembl1282

21. 1-isobutylimidazo[4,5-c]quinolin-4-amine

22. P1qw714r7m

23. 1h-imidazo(4,5-c)quinolin-4-amine, 1-(2-methylpropyl)-

24. 1h-imidazo[4,5-c]quinolin-4-amine, 1-(2-methylpropyl)-

25. Chebi:36704

26. Ncgc00070736-02

27. Zartra

28. Imiquimod Acetate

29. Dsstox_cid_21047

30. Dsstox_rid_79617

31. Dsstox_gsid_41047

32. Aldara (tn)

33. Cas-99011-02-6

34. S 26308

35. Sr-01000611320

36. 1-(2-methylpropyl)-1h-imidazole[4,5-c]quinoline-4-amine

37. Unii-p1qw714r7m

38. Imiquimodum

39. Imiquimod [usan:inn:ban]

40. Vyloma

41. Mtd-39

42. Hsdb 8129

43. Tmx 101

44. Imiquimod,(s)

45. Imiquimod- Bio-x

46. 6t0

47. Imiquimod - Aldara

48. Zyclara (tn)

49. Dz-2636

50. R837

51. Imiquimod [inn]

52. Imiquimod [jan]

53. Imiquimod [mi]

54. Imiquimod [usan]

55. Imiquimod [vandf]

56. Imiquimod [mart.]

57. (non-labelled)imiquimod-d9

58. Imiquimod [usp-rs]

59. Imiquimod [who-dd]

60. Imiquimod (jan/usp/inn)

61. Schembl26136

62. Imiquimod [ema Epar]

63. Mls000083577

64. Bidd:gt0859

65. Gtpl5003

66. Imiquimod [orange Book]

67. Dtxsid7041047

68. Imiquimod [usp Monograph]

69. Hms2090m14

70. Hms2232g07

71. Hms3373b13

72. Hms3715n19

73. Hms3747a13

74. Pharmakon1600-01502351

75. Bcp05151

76. Hy-b0180

77. Tox21_110985

78. Ac-529

79. Bbl010772

80. Bdbm50240849

81. Nsc369100

82. Nsc759651

83. Nsc811538

84. S1211

85. Stk583860

86. Zinc19632912

87. Imiquimod - Cas 99011-02-6

88. Imiquimod, >=98% (hplc), Solid

89. Akos005507352

90. Cellulose, Hydrogen 1,2-benzenedicarboxylate, 2-hydroxypropyl Methyl Ether

91. Tox21_110985_1

92. 1h-imidazo[4, 1-(2-methylpropyl)-

93. Ccg-208015

94. Cs-2058

95. Db00724

96. Ks-5218

97. Nsc 369100

98. Nsc 741062

99. Nsc 759651

100. Nsc-811538

101. Yh44175

102. (hydroxypropyl)methyl Cellulose Phthalate

103. Imiquimod 100 Microg/ml In Acetonitrile

104. Ncgc00070736-03

105. Ncgc00070736-04

106. Bi164576

107. Smr000048307

108. Sy017571

109. Ft-0602727

110. I0747

111. D02500

112. 1-isobutyl-1h-imidazo [4,5-c]quinolin-4-amine

113. 1-isobutyl-1h-imidazo[4,5-c]quinoline-4-amine

114. Ab00399298-05

115. Ab00399298-06

116. Ab00399298-07

117. Ab00399298_08

118. Ab00399298_09

119. 011i026

120. 1-isobutyl-1h-imidazo[4,5-c]quinolin-4-ylamine

121. A845945

122. Q423417

123. 1-(2-methylpropyl)-4-imidazo[4,5-c]quinolinamine

124. Sr-01000611320-2

125. Sr-01000611320-3

126. Brd-k26657438-001-01-2

127. Brd-k26657438-001-13-7

128. 1-(2-methylpropyl)-1himidazo[4,5-c]quinolin-4-amine

129. 1-(2-methylpropyl)-1h-imidazo[4,5-c]-quinolin-4-amine

130. Imiquimod, United States Pharmacopeia (usp) Reference Standard

2.4 Create Date
2005-06-29
3 Chemical and Physical Properties
Molecular Weight 240.30 g/mol
Molecular Formula C14H16N4
XLogP32.6
Hydrogen Bond Donor Count1
Hydrogen Bond Acceptor Count3
Rotatable Bond Count2
Exact Mass240.137496527 g/mol
Monoisotopic Mass240.137496527 g/mol
Topological Polar Surface Area56.7 Ų
Heavy Atom Count18
Formal Charge0
Complexity294
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Drug Information
1 of 6  
Drug NameAldara
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelAldara (imiquimod 5%) Cream is an immune response modifier for topical administration. Each gram contains 50 mg of imiquimod in an off-white oil-in-water vanishing cream base consisting of isostearic acid, cetyl alcohol, stearyl alcohol, white petrol...
Active IngredientImiquimod
Dosage FormCream
RouteTopical
Strength5%
Market StatusPrescription
CompanyMedicis

2 of 6  
Drug NameImiquimod
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelAldara (imiquimod 5%) Cream is an immune response modifier for topical administration. Each gram contains 50 mg of imiquimod in an off-white oil-in-water vanishing cream base consisting of isostearic acid, cetyl alcohol, stearyl alcohol, white petrol...
Active IngredientImiquimod
Dosage FormCream
RouteTopical
Strength5%
Market StatusPrescription
CompanyApotex; Teva Pharms Usa; Taro; Strides Pharma; Glenmark Generics; Fougera Pharms; Tolmar; Perrigo Israel

3 of 6  
Drug NameZyclara
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelZYCLARA (imiquimod) Cream, 2.5% or 3.75% is intended for topical administration. Each gram contains 25 mg or 37.5 mg of imiquimod, respectively, in a white to faintly yellow oil-in-water cream base consisting of isostearic acid, cetyl alcohol, steary...
Active IngredientImiquimod
Dosage FormCream
Routetopical; Topical
Strength3.75%; 2.5%
Market StatusPrescription
CompanyMedicis; Graceway

4 of 6  
Drug NameAldara
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelAldara (imiquimod 5%) Cream is an immune response modifier for topical administration. Each gram contains 50 mg of imiquimod in an off-white oil-in-water vanishing cream base consisting of isostearic acid, cetyl alcohol, stearyl alcohol, white petrol...
Active IngredientImiquimod
Dosage FormCream
RouteTopical
Strength5%
Market StatusPrescription
CompanyMedicis

5 of 6  
Drug NameImiquimod
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelAldara (imiquimod 5%) Cream is an immune response modifier for topical administration. Each gram contains 50 mg of imiquimod in an off-white oil-in-water vanishing cream base consisting of isostearic acid, cetyl alcohol, stearyl alcohol, white petrol...
Active IngredientImiquimod
Dosage FormCream
RouteTopical
Strength5%
Market StatusPrescription
CompanyApotex; Teva Pharms Usa; Taro; Strides Pharma; Glenmark Generics; Fougera Pharms; Tolmar; Perrigo Israel

6 of 6  
Drug NameZyclara
PubMed HealthImiquimod (On the skin)
Drug ClassesImmune Modulator
Drug LabelZYCLARA (imiquimod) Cream, 2.5% or 3.75% is intended for topical administration. Each gram contains 25 mg or 37.5 mg of imiquimod, respectively, in a white to faintly yellow oil-in-water cream base consisting of isostearic acid, cetyl alcohol, steary...
Active IngredientImiquimod
Dosage FormCream
Routetopical; Topical
Strength3.75%; 2.5%
Market StatusPrescription
CompanyMedicis; Graceway

4.2 Therapeutic Uses

Adjuvants, Immunologic; Antineoplastic Agents

National Library of Medicine's Medical Subject Headings online file (MeSH, 2013)


Imiquimod is used topically for the treatment of clinically typical, nonhyperkeratotic, nonhypertrophic actinic keratosis on the face or scalp in immunocompetent adults; treatment of biopsy-confirmed, primary superficial basal cell carcinoma in immunocompetent adults; and treatment of external genital and perianal exophytic warts (condylomata acuminata) caused by human papillomavirus (HPV). /Included in US product label/

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3577


Topical imiquimod has been effective when used in a limited number of adults and children for the treatment of molluscum contagiosum. /NOT included in US product label/

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3578


Imiquimod 5% cream has been used for the topical treatment of external genital and perianal HPV warts in a limited number of adults with human immunodeficiency virus (HIV) infection; however, the response rate appears to be lower in these individuals than in those who are not HIV infected. /NOT included in US product label/

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3578


For more Therapeutic Uses (Complete) data for Imiquimod (6 total), please visit the HSDB record page.


4.3 Drug Warning

Adverse local reactions, including erythema, erosion, excoriation/flaking, and edema, commonly occur at the site of application of imiquimod and/or surrounding areas. These reactions usually are mild to moderate in severity; however, severe local reactions have been reported.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3578


In controlled studies in adults with actinic keratosis, the most frequently reported local skin reactions in those receiving imiquimod 5% cream (twice weekly for 16 weeks) were erythema (97%), flaking/scaling/dryness (93%), scabbing/crusting (79%), edema (49%), erosion/ulceration (48%), weeping/exudate (22%), and vesicles (9%).1 Application site reactions (e.g., bleeding, burning, induration, irritation, pain, pruritus, stinging, tenderness) occurred in 33% of those receiving topical imiquimod compared with 14% of those receiving placebo. In these studies, 16% of patients discontinued imiquimod treatment because of local or application site reactions and 91% of these were able to resume treatment after a rest period.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3578


Adverse dermatologic reactions at sites away from the site of application have been reported in some patients receiving topical imiquimod. Remote site reactions have included bleeding, burning, edema, erosion, erythema, excoriation/flaking, induration, pain, pruritus, tenderness, tinea cruris, and ulceration.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3579


When imiquimod 5% cream was used in controlled studies in patients with genital and perianal HPV warts (3 times weekly for up to 16 weeks), erythema occurred in 58-65%, erosion in 30-31%, excoriation/flaking in 18-26%, edema in 12-18%, scabbing in 4-13%, induration in 5-7%, ulceration in 4-8%, and vesicles in 2-3% of those receiving the drug.1 In addition, application site reactions in those receiving the drug included pruritus (22-32%), burning (9-26%), pain (2-8%), and soreness (0-3%). In addition, fungal infections occurred in 2-11% of patients receiving the drug. Overall, 1.2% of patients in these studies discontinued treatment because of local or application site reactions.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3579


For more Drug Warnings (Complete) data for Imiquimod (25 total), please visit the HSDB record page.


4.4 Drug Indication

For the topical treatment of clinically typical, nonhyperkeratotic, nonhypertrophic actinic keratoses on the face or scalp in immunocompetent adults. Also indicated for the treatment of external genital and perianal warts/condyloma acuminata in individuals 12 years old and above.


FDA Label


Zyclara is indicated for the topical treatment of clinically typical, non-hyperkeratotic, non-hypertrophic, visible or palpable actinic keratosis of the full face or balding scalp in immunocompetent adults when other topical treatment options are contraindicated or less appropriate.


Imiquimod cream is indicated for the topical treatment of:

- external genital and perianal warts (condylomata acuminata) in adults;

- small superficial basal-cell carcinomas (sBCCs) in adults;

- clinically typical, non-hyperkeratotic, non-hypertrophic actinic keratoses (AKs) on the face or scalp in immunocompetent adult patients when size or number of lesions limit the efficacy and / or acceptability of cryotherapy and other topical treatment options are contraindicated or less appropriate.


Imiquimod cream is indicated for the topical treatment of external genital and perianal warts (condyloma acuminata) in adult patients.


5 Pharmacology and Biochemistry
5.1 Pharmacology

Imiquimod is an immune response modifier that acts as a toll-like receptor 7 agonist. Imiquimod is commonly used topically to treat warts on the skin of the genital and anal areas. Imiquimod does not cure warts, and new warts may appear during treatment. Imiquimod does not fight the viruses that cause warts directly, however, it does help to relieve and control wart production. It is not used on warts inside the vagina, penis, or rectum. Imiquimod is also used to treat a skin condition of the face and scalp called actinic keratoses. Imiquimod can also be used to treat certain types of skin cancer called superficial basal cell carcinoma. Imiquimod is particularly useful on areas where surgery or other treatments may be difficult, complicated or otherwise undesirable, especially the face and lower legs.


5.2 MeSH Pharmacological Classification

Adjuvants, Immunologic

Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity. (See all compounds classified as Adjuvants, Immunologic.)


Antineoplastic Agents

Substances that inhibit or prevent the proliferation of NEOPLASMS. (See all compounds classified as Antineoplastic Agents.)


Interferon Inducers

Agents that promote the production and release of interferons. They include mitogens, lipopolysaccharides, and the synthetic polymers Poly A-U and Poly I-C. Viruses, bacteria, and protozoa have been also known to induce interferons. (See all compounds classified as Interferon Inducers.)


5.3 FDA Pharmacological Classification
5.3.1 Active Moiety
IMIQUIMOD
5.3.2 FDA UNII
P1QW714R7M
5.3.3 Pharmacological Classes
Increased Cytokine Production [PE]; Interferon Inducers [MoA]; Increased Cytokine Activity [PE]
5.4 ATC Code

D06BB10


D06BB10


L03AX


D06BB10

S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355


D - Dermatologicals

D06 - Antibiotics and chemotherapeutics for dermatological use

D06B - Chemotherapeutics for topical use

D06BB - Antivirals

D06BB10 - Imiquimod


5.5 Absorption, Distribution and Excretion

Absorption

Well absorbed through skin (as a cream)


Following topical application to the skin in adults with actinic keratosis (75-mg doses 3 times weekly for 16 weeks), 0.08-0.15% of the dose is eliminated in urine as unchanged drug and metabolites. Following topical application in patients with HPV warts, 0.11 or 2.41% of the dose is eliminated in urine as unchanged drug and metabolites in men or women, respectively.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3580


Imiquimod is absorbed systemically following topical application to skin. In adults with actinic keratosis who received topical imiquimod 5% cream 3 times weekly for 16 weeks, mean peak serum concentrations at the end of week 16 were approximately 0.1, 0.2, or 3.5 ng/mL in those treated on the face (12.5-mg doses), scalp (25-mg doses), or hands/arms (75-mg doses), respectively. Systemic exposure appeared to depend more on the surface area of the application site than on the total applied dose. In patients with external genital and perianal human papillomavirus (HPV) warts who received topical imiquimod 5% cream (average dose 4.6 mg), mean peak serum concentrations were 0.4 ng/mL.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3580


5.6 Biological Half-Life

20 hours (topical dose), 2 hours (subcutaneous dose)


Studies using subcutaneous imiquimod indicate the drug has an apparent half-life of 2 hours. Following topical application, imiquimod appears to be retained in the skin for prolonged periods since the half-life is approximately 10 times greater than that reported following subcutaneous administration.

American Society of Health-System Pharmacists 2012; Drug Information 2012. Bethesda, MD. 2012, p. 3580


5.7 Mechanism of Action

Imiquimod's mechanism of action is via stimulation of innate and acquired immune responses, which ultimately leads to inflammatory cell infiltration within the field of drug application followed by apoptosis of diseased tissue. Imiquimod does not have direct antiviral activity. Studies of mice show that imiquimod may induce cytokines, including interferon-alpha (IFNA) as well as several IFNA genes (IFNA1, IFNA2, IFNA5, IFNA6, and IFNA8) as well as the IFNB gene. Imiquimod also induced the expression of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha genes. In the treatment of basal cell carcinoma, Imiquimod appears to act as a toll-like receptor-7 agonist, and is thought to exert its anti-tumor effect via modification of the immune response and stimulation of apoptosis in BCC cells. In treating basal cell carcinoma it may increase the infiltration of lymphocytes, dendritic cells, and macrophages into the tumor lesion.


Imiquimod and resiquimod represent Toll-like receptor (TLR) 7 and 8 agonists, which emerged as attractive candidates for tumor therapy. To elucidate immune cells, which mainly contribute to TLR7/8-mediated antitumoral activity, /the researchers/ investigated the impact of imiquimod and resiquimod on native human 6-sulfo LacNAc (slan) dendritic cells (DCs). /The researchers/ found that both TLR7/8 agonists significantly improve the release of various proinflammatory cytokines by slanDCs and promote their tumor-directed cytotoxic activity. Furthermore, resiquimod efficiently augmented the ability of slanDCs to stimulate T cells and natural killer cells. These results indicate that imiquimod and resiquimod trigger various immunostimulatory properties of slanDCs, which may contribute to their antitumor effects.

PMID:23402811 Jahnisch H et al; Cancer Lett. 2013 Feb 9 (Epub ahead of print)


Aldara is a cream used for topical treatment of non-melanoma skin cancer, and is thought to act through stimulation of anti-tumour immunity. The active ingredient, imiquimod, has been shown to stimulate toll-like receptor 7. Aldara also induces psoriasis-like lesions when applied to naive murine skin, and as such is used as a mouse model for psoriasis. Here we find that in naive murine skin, Aldara induces inflammation largely independently of toll-like receptor 7. Surprisingly, inflammasome activation, keratinocyte death and interleukin 1 release also occur in response to the vehicle cream in the absence of imiquimod. We show that isostearic acid, a major component of the vehicle, promotes inflammasome activation in cultured keratinocytes, and so may contribute to the observed effects of Aldara on murine skin. Aldara therefore stimulates at least two immune pathways independently, and both imiquimod and vehicle are required for a full inflammatory response. Although it remains to be tested, it is possible that imiquimod-independent effects also contribute to the therapeutic efficacy of Aldara.

PMID:23463003 Walter A et al; Nat Commun. 2013 Mar 5;4:1560


Imiquimod is recognized as an agonist for Toll-like receptor 7 (TLR7) in immunocompetent cells. TLR7, as well as TLR3 and TLR8, triggers the immune responses, such as the production of type I interferons (IFNs) and proinflammatory cytokines via recognition of viral nucleic acids in the infected cells. In this study, /the reseachers/ proposed that imiquimod has an IFN-independent antiviral effect in nonimmune cells. Imiquimod, but not resiquimod, suppressed replication of human herpes simplex virus 1 (HSV-1) in FL cells. We analyzed alternation of gene expression by treatment with imiquimod using microarray analysis. Neither type I IFNs, nor TLRs, nor IFN-inducible antiviral genes were induced in imiquimod-treated FL cells. Cystatin A, a host cysteine protease inhibitor, was strongly upregulated by imiquimod and took a major part in the anti-HSV-1 activity deduced by the suppression experiment using its small interfering RNA. Upregulation of cystatin A was suggested to be mediated by antagonizing adenosine receptor A(1) and activating the protein kinase A pathway. Imiquimod, but not resiquimod, was shown to interact with adenosine receptor A(1). Imiquimod-induced anti-HSV-1 activity was observed in other cells, such as HeLa, SiHa, and CaSki cells, in a manner consistent with the cystatin A induction by imiquimod. These results indicated that imiquimod acted as an antagonist for adenosine receptor A(1) and induced a host antiviral protein, cystatin A. The process occurred independently of TLR7 and type I IFNs.

PMID:22787201 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3457300 Kan Y et al; J Virol 86 (19): 10338-46 (2012)


Toll-like receptor (TLR) agonists have anticancer effect by inducing apoptosis or activating immune cells. In this study, we investigated whether imiquimod, TLR7 agonist, inhibits the proliferation of oral cancer cells. Toll-like receptor 7 expression and IL-6/8 production by imiquimod were examined using RT-PCR and Enzyme-linked immunosorbent assay, respectively. Cell viability was examined by MTT assay. To examine apoptotic cell death, Annexin V/PI staining for flow cytometry and Western blot analysis were performed. Necrotic cell death was determined by leakage of lactate dehydrogenase (LDH), HMGB1, and PI staining in imiquimod-treated oral squamous cell carcinoma (OSCC) cells. Toll-like receptor 7 mRNA was expressed in OSCC cells. Imiquimod induced IL-6 and IL-8 production in OSCC cells, suggesting the functional expression of TLR7. Imiquimod inhibited cells proliferation in a dose-dependent manner. The ratio of annexin V-positive cells and cleaved caspase-3/7 was increased by imiquimod treatment in OSCC cells, suggesting that imiquimod-induced cell death in OSCC cells may be owing to apoptosis. In addition, LDH secretion and PI staining were detected in OSCC cells treated with imiquimod, showing that imiquimod also induced necrotic cell death in the OSCC cells. Imiquimod inhibited effectively the growth of OSCC cells by inducing apoptosis and necrosis.

PMID:22577802 Ahn MY et al; J Oral Pathol Med 41 (7): 540-6 (2012)


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16-Jan-2021
30-Sep-2024
KGS
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