Imiquimod

240.3

240.30

1592732-453-0

P1QW714R7M

759651|369100

DTXSID7041047

C1431

Crystals from DMF

D06BB10|L03AX|D - Dermatologicals

2933990090

56.7

2.6

1

1.3±0.1 g/cm3

292-294 °C

456.7°C at 760 mmHg

230.0±29.6 °C

1.681

soluble in dimethyl sulfoxide and dimethyl formamide. Slightly soluble in water. Insoluble in ethanol.DMSO: soluble

Store at +4°C

7.82X10-9 mm Hg at 25 deg C (est)

Henry's Law constant = 8.26X10-13 atm-cu m/mol at 25 °C (est)

Ⅲ

6.1

UN28116.1/PG3

3

25-36/37/38

26-45-36/37/39-27

NJ5903450

T,Xi

Incompatible with strong oxidizing agents.

P261-P264-P301 + P310-P305 + P351 + P338

H300-H315-H319-H335

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|Place material in a thick plastic hazardous waste disposal bag or leakproof container and label it CAUTION: HAZARDOUS CHEMICAL WASTE. Dispose of waste in accordance with all applicable Federal, State and local laws.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including imiquimod, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

H413 (100%): May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]|P273, and P501|Aggregated GHS information provided by 2 companies from 2 notifications to the ECHA C&L Inventory.| |Danger|H300 (88.64%): Fatal if swallowed [Danger Acute toxicity, oral]|P261, P264, P270, P271, P280, P301+P310, P302+P352, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 45 companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Airborne exposure should be controlled primarily by engineering controls such as general dilution ventilation, local exhaust ventilation, or process enclosure. Local exhaust ventilation is generally preferred to general exhaust because it can control the contaminant at its source, preventing dispersion into the work area. An industrial hygiene survey involving air monitoring may be used to determine the effectiveness of engineering controls. Effectiveness of engineering controls intended for use with highly potent materials should be assessed by use of nontoxic surrogate materials. Local exhaust ventilation such as a laboratory fume hood or other vented enclosure is recommended, particularly for grinding, crushing, weighing, or other dust-generating procedures.|Respiratory Protection: Where respirators are deemed necessary to reduce or control occupational exposures, use NIOSH-approved respiratory protection and have an effective respirator program in place. Gloves: Chemically compatible. For handling solutions, ensure that the glove material is protective against the solvent being used. Use handling practices that minimize direct hand contact. Employees who are sensitive to natural rubber (latex) should use nitrile or other synthetic nonlatex gloves. Use of powdered latex gloves should be avoided due to the risk of latex allergy. Eye Protection: Safety glasses with sideshields are recommended. Face shields or goggles may be required if splash potential exists or if corrosive materials are present. Approved eye protection (e.g., bearing the ANSI Z87 or CSA stamp) is preferred. Maintain eyewash facilities in the work area. Protective Clothing: For handling of laboratory scale quantities, a cloth lab coat is recommended. Where significant quantities are handled, work clothing may be necessary to prevent take-home contamination.

This material is assumed to be combustible.

Water spray, dry chemical, carbon dioxide or foam as appropriate for surrounding fire and materials.|As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing.

Wear approved respiratory protection, chemically compatible gloves and protective clothing. Wipe up spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately labeled container for disposal. Wash spill site.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|As with all dry powders it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.|As a general rule, when handling USP Reference Standards, avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Clean equipment and work surfaces with suitable detergent or solvent after use. After removing gloves, wash hands and other exposed skin thoroughly.|Avoid exposure to heat and moisture.

Moderate to severe irritant to the skin and eyes.

Symptoms of overdose include flu-like symptoms, such as fever, fatigue, headache, nausea, diarrhoea and muscle pain.

Imiquimod cream should be used with caution in organ transplant patients. Consideration should be given to balancing the benefit of imiquimod treatment for these patients with the risk associated with the possibility of organ rejection or graft-versus-host disease.|Imiquimod should be used with caution in patients with reduced hematologic reserve.|Imiquimod cream should be used with caution in patients with autoimmune conditions. Consideration should be given to balancing the benefit of imiquimod treatment for these patients with the risk associated with a possible worsening of their autoimmune conditions.

Imiquimod's production and use as an immunologic adjuvant and antineoplastic agent(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1000(SRC), determined from a structure estimation method(2), indicates that imiquimod is expected to have moderate mobility in soil(SRC). Aromatic amines are expected to bind strongly to humus or organic matter in soils due to the high reactivity of the aromatic amino group(3,4), suggesting that mobility may be much lower in some soils(SRC). Volatilization of imiquimod from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 8.3X10-12 atm-cu m/mole(SRC), using a fragment constant estimation method(5). Imiquimod is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.8X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2013).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1000(SRC), determined from a structure estimation method(2), indicates that imiquimod is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 8.3X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 50(SRC), from an estimated log Kow of 3.06(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data in water were not available(SRC, 2013).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), imiquimod, which has an estimated vapor pressure of 7.8X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase imiquimod may be removed from the air by wet and dry deposition(SRC). Imiquimod contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Imiquimod is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Imiquimod contains chromophores that absorb at wavelengths >290 nm(1) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 50 was calculated in fish for imiquimod(SRC), using an estimated log Kow of 3.06(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of imiquimod can be estimated to be 1000(SRC). According to a classification scheme(2), this estimated Koc value suggests that imiguimod is expected to have low mobility in soil. Aromatic amines are expected to bind strongly to humus or organic matter in soils due to the high reactivity of the aromatic amino group(3,4), suggesting that mobility may be much lower in some soils(SRC).

The Henry's Law constant for imiquimod is estimated as 8.3X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that imiquimod is expected to be essentially nonvolatile from water and moist soil surfaces(2). Imiquimod is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.8X10-9 mm Hg(SRC), determined from a fragment constant method(3).

Occupational exposure to imiquimod may occur through inhalation and dermal contact with this compound at workplaces where imiquimod is produced or used. Exposure to imiquimod among the general population may be limited to those administered this drug. (SRC)

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.|Drug: Imiquimod

Adjuvants, Immunologic; Antineoplastic Agents|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/|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/|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/|For more Therapeutic Uses (Complete) data for Imiquimod (6 total), please visit the HSDB record page.

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

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.

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

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.|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.

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.

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.|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.|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.|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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Topical overdosing of Aldara Cream could result in an increased incidence of severe local skin reactions and may increase the risk for systemic reactions. The most clinically serious adverse event reported following multiple oral imiquimod doses of >200 mg (equivalent to imiquimod content of >16 packets) was hypotension, which resolved following oral or intravenous fluid administration.|/CASE REPORTS/ Erosive pustular dermatosis of the scalp (EPDS) is a rare condition characterized by sterile pustules, erosions, and crusted lesions on the scalp of elderly patients. This inflammatory disorder has an unknown origin and it could develop into areas of alopecia that tend to be atrophic. An 84-year-old Caucasian man presented with a several months history of painful erythematous erosions and crusts on his scalp. The lesions appeared after treatment with imiquimod cream for actinic keratoses. Previous therapies included topical antibiotics and topical steroids. Physical examination revealed the presence of extensive erosions and crusts on the scalp, with minute pustules on the sides. The clinical features and the medical history led us to the diagnosis of EPDS. Treatment with systemic steroid was administered with improvement observed after ten days. The clinical manifestations of EPDS completely resolved after 2 months, without clinical relapses.|/CASE REPORTS/ Imiquimod is a topical immune response modifier used to treat anogenital warts. Although considered a safe drug, mild to moderate local and systemic side-effects may occasionally occur. /The researchers/ report three cases of local and systemic adverse effects related to imiquimod, including one case that mimicked meningitis, which promptly resolved with drug cessation.|/CASE REPORTS/ A 44-year-old man who was previously diagnosed with actinic cheilitis was prescribed imiquimod cream 5%, which resulted in thick hemorrhagic crusting of the lower lip after 4 applications. He subsequently noted the development of lichen planus lesions on his arms and legs for the first time in 15 years following imiquimod use. On follow-up he also was noted to have characteristic Wickham striae on his lower lip. Lichen planus is an autoimmune inflammatory condition in which autoreactive T lymphocytes attack keratinocytes. The mechanism of action for imiquimod is upregulation of IFN-alpha and IFN-beta. Treatment with clobetasol cream 0.05% led to resolution of his lichen planus lesions.|For more Human Toxicity Excerpts (Complete) data for Imiquimod (6 total), please visit the HSDB record page.

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

For topical use, imiquimod is commercially /available/ as a 5% cream. Each gram of the cream contains 50 mg of imiquimod in an off-white, oil-in-water vanishing cream base. Imiquimod topical cream contains methylparaben and propylparaben as preservatives.|Topical: Cream 5%, Aldara (Graceway).|Zyclara, Beselna

Cellulose, hydrogen 1,2-benzenedicarboxylate, 2-hydroxypropyl methyl ether: ACTIVE|XU - indicates a substance exempt from reporting under the Chemical Data Reporting Rule, (40 CFR 711).

Human drugs -> Zyclara -> EMA Drug Category|Antibiotics and chemotherapeutics for dermatological use -> Human pharmacotherapeutic group|Human drugs -> Aldara -> EMA Drug Category|Human drugs -> Zartra -> EMA Drug Category|Immunostimulants -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients