Registered Kenya · PPB

TRIMICON

TRIAMCINOLONE ACETONIDE/MICONAZOLE NITRATE

H2009/20811/580 TRIAMCINOLONE ACETONIDE 0.2%WW/MICONAZOLE NITRATE 2% alimentary tract and metabolism INN generic

What it does

Acetonide is a medication used to reduce inflammation and treat various skin conditions.

Commonly used for: skin inflammation, eczema, dermatitis, allergic reactions

Read more in plain English ↓

Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.

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Registration & product details

Registration no.
H2009/20811/580
Registration date
-
Expiry date
-
Status
Registered
Active ingredient
TRIAMCINOLONE ACETONIDE/MICONAZOLE NITRATE
Strength
-
Pack size
-
Therapeutic class
-
ATC class (WHO)
A01AB - Antiinfectives and antiseptics for local oral treatment
RxNorm RxCUI
6932
Manufacturer / MAH
Omaera Pharmaceuticals
Applicant / LTR
-
Country of origin
FOREIGN
Manufacturer location
Zaf Holding Godowns, Next to Twiga Construction Ltd, Baba Dogo Rd, Nairobi, Kenya

Source: Pharmacy and Poisons Board · fetched 2026-01-28 22:11:41 · updated 2026-03-23 04:56:52

Drug Interactions

85
Check interactions

Pharmacodynamic Warnings

Triamcinolone appears in TABLE 17: Drugs that reduce serum potassium

Severe (6)

Antihistamines,non-Sedating - increases exposure

Miconazole is predicted to increase the exposure to antihistamines, non-sedating (mizolastine). Avoid.

Severe Theoretical

Ergometrine - increases exposure

Miconazoleispredictedtoincreasetheexposureto ergometrine.Avoid.oTheoretical

Severe Theoretical

Ergotamine - increases exposure

Miconazoleispredictedtoincreasetheexposureto ergotamine.Avoid.oTheoretical

Severe Theoretical

Mifamurtide - decreases efficacy

Corticosteroidsarepredictedtodecreasetheefficacyof mifamurtide.Avoid.rTheoretical

Severe Theoretical

Mizolastine - increases exposure

Miconazole is predicted to increase the exposure to antihistamines, non-sedating (mizolastine). Avoid.

Severe Theoretical

Oral Benzodiazepines - increases exposure

Miconazole is predicted to increase the exposure to oral benzodiazepines (midazolam). Avoid.

Severe Theoretical

Moderate (53)

Alfentanil - increases exposure

Miconazole is predicted to increase the exposure to opioids (alfentanil). Use with caution and adjust dose.

Moderate Theoretical

Alkylating Agents - increases concentration

Miconazole is predicted to increase the concentration of alkylating agents (busulfan). Use with caution and adjust dose.

Moderate Theoretical

Alprazolam - increases exposure

Miconazole is predicted to increase the exposure to benzodiazepines (alprazolam). Use with caution and adjust dose.

Moderate Theoretical

Amlodipine - increases exposure

Miconazole is predicted to increase the exposure to calcium channel blockers (amlodipine, felodipine, lacidipine, lercanidipine, nicardipine, nifedipine, nimodipine, verapamil). Use with caution and a

Moderate Theoretical

Antiarrhythmics - increases exposure

Miconazole is predicted to increase the exposure to antiarrhythmics (disopyramide). Use with caution and adjust dose.

Moderate Theoretical

Unknown (26)

Aminoglycosides - decreases exposure

Miconazole potentially decreases the exposure to aminoglycosides (tobramycin).

Unknown Anecdotal

Aspirin - decreases concentration

Corticosteroids are predicted to decrease the concentration of aspirin (high-dose) and aspirin (high-dose) increases the risk of gastrointestinal bleeding when given with corticosteroids.

Unknown Study

Choline Salicylate - decreases concentration

Corticosteroids are predicted to decrease the concentration of cholinesalicylate. Ciclesonide → see corticosteroids Ciclosporin → see TABLE 2 p. 1517 (nephrotoxicity), TABLE 16 p. 1521 (increased seru

Unknown Study

Cobimetinib - increases exposure

Miconazoleispredictedtoincreasetheexposureto cobimetinib.rTheoretical

Unknown Theoretical

Corticosteroids - increases exposure

Cobicistat is predicted to increase the exposure to corticosteroids (beclometasone) (risk with beclometasone is likely to be lower than with other corticosteroids).

Unknown Theoretical

Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact

Disclaimer: This information is sourced from Pharmacy and Poisons Board (Kenya). Always consult a qualified healthcare professional before using any medication.

About acetonide

Acetonide is a medication used to reduce inflammation and treat various skin conditions.

What it treats

  • skin inflammation
  • eczema
  • dermatitis
  • allergic reactions

How it works

Acetonide works by decreasing swelling, redness, and itching in the affected area.

Who it's for

This medication is suitable for adults and children with certain skin conditions.

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

About miconazole

Miconazole is an antifungal medication used to treat fungal infections on the skin and in the mouth.

What it treats

  • fungal infections of the skin
  • oral thrush (fungal infection in the mouth)

How it works

It works by stopping the growth of fungi, helping to clear the infection.

Who it's for

This medication is for adults and children who have fungal infections.

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

About triamcinolone

Triamcinolone is a corticosteroid used to reduce inflammation and treat various conditions.

What it treats

  • inflammation
  • allergic reactions
  • skin disorders
  • asthma
  • arthritis

How it works

It works by suppressing the immune system to reduce inflammation and allergic responses.

Who it's for

Triamcinolone is for people with conditions that involve inflammation or an overactive immune response.

Drug class

Corticosteroids

Cautions

  • • Be cautious if you are taking other medications that lower potassium levels.

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

Clinical monograph: Miconazole

BNF-referenced

Miconazole is an azole antifungal agent utilized for the treatment of various fungal infections, particularly those caused by Candida species. It acts primarily by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes, thereby compromising the integrity and function of the fungal cell. Miconazole can be administered topically, orally, or intravaginally, making it versatile for treating conditions such as oropharyngeal candidiasis, vaginal candidiasis, and superficial skin infections.

Indications

  • Vaginal candidiasis
  • Oropharyngeal candidiasis
  • Vulvovaginal infections
  • Superficial fungal infections

Dosage

Adults: For vaginal candidiasis, miconazole cream is typically applied twice daily, using 5 g inserted into the vagina for 7 days. For oropharyngeal candidiasis, the oral gel is usually administered as 2.5 mL four times a day.

Mechanism of action

Miconazole primarily acts through the inhibition of the CYP450 14α-lanosterol demethylase enzyme, leading to disrupted ergosterol production in fungal cell membranes. This disruption results in increased cell membrane permeability and leakage of essential cellular constituents. Additionally, miconazole inhibits fungal peroxidase and catalase, increasing the production of reactive oxygen species (ROS) which contribute to fungal cell death. Miconazole also elevates intracellular levels of farnesol, which disrupts quorum sensing in Candida, preventing the transition to more virulent forms.

Pharmacodynamics

Miconazole is predominantly applied topically, leading to minimal systemic absorption. Its primary adverse reactions are usually localized to hypersensitivity reactions, with the potential for anaphylaxis in rare cases. Patients using intravaginal miconazole are advised to avoid reliance on other contraceptive methods and not to use tampons simultaneously due to the risk of altered vaginal flora.

Pharmacokinetics

Miconazole is poorly absorbed when applied topically or intravaginally, resulting in low systemic exposure. The pharmacokinetics of miconazole can vary based on the route of administration, but systemic absorption is generally low, thus limiting systemic side effects and interactions. Miconazole is extensively metabolized in the liver, and its metabolites are excreted primarily through the urine.

Contra-indications

  • Hypersensitivity to miconazole or any of its excipients
  • Recent arterial thromboembolic disease (e.g. angina, myocardial infarction)
  • Undiagnosed vaginal bleeding
  • Oestrogen-dependent tumors (e.g. breast cancer in first-degree relatives)
  • Acute porphyrias
  • Severe diabetes (increased risk of heart disease)

Adverse effects

  • Dysmenorrhoea
  • Skin reactions
  • Increased risk of gallbladder disease
  • Migraine or migraine-like headaches
  • Abdominal pain
  • Dysuria
  • Nausea
  • Pelvic cramps
  • Vaginal hemorrhage
  • Angioedema

Interactions

  • Miconazole + antihistamines (non-sedating): Severe (increases exposure)
  • Miconazole + mizolastine: Severe (increases exposure)
  • Miconazole + oral benzodiazepines: Severe (increases exposure)
  • Miconazole + ergometrine: Severe (increases exposure)
  • Miconazole + ergotamine: Severe (increases exposure)
  • Miconazole + alkylating agents: Moderate (increases concentration)
  • Miconazole + busulfan: Moderate (increases concentration)
  • Miconazole + antiarrhythmics: Moderate (increases exposure)
  • Miconazole + disopyramide: Moderate (increases exposure)
  • Miconazole + benzodiazepines: Moderate (increases exposure)

Precautions

  • Caution in patients with history of breast cancer
  • Monitor breast status regularly in women on oestrogen therapy
  • Risk of endometrial cancer with prolonged use of oestrogens
  • Risk of ovarian cancer with long-term use of combined HRT
  • Increased risk of venous thromboembolism in women using combined or oestrogen-only HRT

Pregnancy

Pregnant women may require a longer duration of treatment, usually about 7 days, to clear the infection. Caution is advised.

Breast-feeding

Manufacturer advises caution; no specific information available.

BNF 85 (British National Formulary) p.930 BNF 85 (British National Formulary) p.1356 BNF 85 (British National Formulary) p.1371 BNF for Children 2019-2020 p.756 BNF for Children 2019-2020 p.771 PubChem / pathway

AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.

Clinical monograph: acetonide

Acetonide is a synthetic corticosteroid used primarily for its anti-inflammatory and immunosuppressive properties. It is often utilized in dermatological preparations to treat various skin conditions due to its ability to reduce inflammation and suppress immune responses. Acetonide can be found in formulations for topical administration and is effective in conditions such as eczema, psoriasis, and contact dermatitis.

Indications

  • Eczema
  • Psoriasis
  • Contact dermatitis
  • Allergic dermatitis
  • Seborrheic dermatitis

Dosage

Children: Refer to specific product information or clinical guidelines for appropriate dosing in children, as it varies by formulation and condition treated.

Adults: Refer to specific product information or clinical guidelines for appropriate dosing, as it varies by formulation and condition treated.

Mechanism of action

Acetonide exerts its effects by binding to glucocorticoid receptors in the cytoplasm of target cells, leading to the translocation of the receptor-ligand complex into the nucleus. This complex then influences the expression of specific genes, resulting in decreased production of pro-inflammatory cytokines and increased production of anti-inflammatory proteins. This modulation of gene expression contributes to its anti-inflammatory and immunosuppressive effects.

Pharmacodynamics

The pharmacodynamics of acetonide involve its ability to inhibit the migration of leukocytes to sites of inflammation, reduce the production of inflammatory mediators such as prostaglandins and leukotrienes, and suppress the immune response. The potency and duration of action can vary based on the specific formulation and concentration used.

Pharmacokinetics

Acetonide is absorbed through the skin when applied topically, with systemic absorption depending on the formulation, application area, and duration of use. It undergoes hepatic metabolism, and its metabolites are excreted primarily through the urine. The half-life and clearance rates can vary based on individual patient factors and specific formulations.

Contra-indications

  • Hypersensitivity to acetonide or any component of the formulation.
  • Active or untreated infections at the site of application.

Adverse effects

  • Local irritation or burning sensation at the application site.
  • Skin thinning or atrophy with prolonged use.
  • Systemic effects such as adrenal suppression with high doses or prolonged therapy.

Interactions

  • Increased risk of systemic effects when used with other corticosteroids.
  • Potentially altered metabolism when administered with CYP3A4 inhibitors or inducers.

Precautions

  • Use with caution in patients with a history of tuberculosis or other infections.
  • Monitor for signs of adrenal insufficiency in patients on high doses.
  • Avoid application to large areas of the body or under occlusive dressings.

Pregnancy

Acetonide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult with a healthcare professional before use.

Breast-feeding

Limited data available. Use with caution as it may be excreted in breast milk. Consult with a healthcare professional before use.

Storage

Store at room temperature, away from direct sunlight and moisture. Keep out of reach of children.

Formulations

  • Topical cream
  • Topical ointment
  • Topical solution

AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.

Clinical monograph: triamcinolone

BNF-referenced

Triamcinolone is a synthetic corticosteroid that exhibits potent anti-inflammatory properties. It is used in various clinical conditions to reduce inflammation and suppress immune responses. As a member of the glucocorticoid family, triamcinolone acts by modulating gene expression and inhibiting the synthesis of inflammatory mediators. Its therapeutic applications include treatment of diseases like asthma, allergies, autoimmune disorders, and dermatological conditions among others.

Indications

  • Asthma
  • Allergic rhinitis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Dermatitis
  • Psoriasis
  • Inflammatory bowel disease

Dosage

Children: Refer to BNF for Children for specific dosing recommendations based on condition and formulation.

Adults: Refer to BNF for specific dosing recommendations based on condition and formulation.

Mechanism of action

Triamcinolone inhibits phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes. This action reduces the formation of arachidonic acid, leading to decreased expression of cyclooxygenase and lipoxygenase, which inhibits the synthesis of prostaglandins and leukotrienes. Additionally, triamcinolone inhibits nuclear factor kappa-B, reducing pro-inflammatory signals such as interleukin-6 and interleukin-8. It interacts with specific intracellular receptor proteins to alter the expression of corticosteroid-responsive genes, leading to the synthesis of proteins like lipocortin that further inhibit inflammatory pathways.

Pharmacodynamics

Triamcinolone exhibits significant anti-inflammatory effects through multiple mechanisms, including suppression of immune cell migration and modulation of inflammatory mediator production. Its effects can lead to reduced edema, erythema, and pain associated with inflammatory processes. The drug’s action is mediated by its ability to influence gene expression in target tissues, resulting in a broad range of effects on the immune response and inflammation.

Pharmacokinetics

Triamcinolone is well absorbed following parenteral administration, with peak plasma concentrations typically observed within a few hours. It has a relatively long half-life, which allows for sustained therapeutic effects. The drug is metabolized primarily in the liver and excreted via the kidneys. Its pharmacokinetic profile may vary depending on the route of administration and the specific formulation used.

Interactions

  • mitotane+triamcinolone: Moderate (decreases exposure)
  • rifampicin+triamcinolone: Moderate (decreases exposure)
  • cobicistat+triamcinolone: Unknown (increases exposure)
  • idelalisib+triamcinolone: Unknown (increases exposure)
  • clarithromycin+triamcinolone: Unknown (increases exposure)

Pregnancy

Corticosteroids, including triamcinolone, should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. They may cause fetal harm, particularly when used in high doses or for prolonged periods in the second and third trimesters.

Breast-feeding

Triamcinolone is excreted in human milk, and caution should be exercised when administering to nursing mothers. The benefits of breastfeeding should be weighed against the potential risk of adverse effects on the infant.

Storage

Store at room temperature, away from light and moisture. Do not freeze.

AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.

Molecular reference: Miconazole

PubChem CID 4189

Molecular formula: C18H14Cl4N2O

Mechanism of action

Miconazole is an azole antifungal used to treat a variety of conditions, including those caused by _Candida_ overgrowth. Unique among the azoles, miconazole is thought to act through three main mechanisms. The primary mechanism of action is through inhibition of the CYP450 14α-lanosterol demethylase enzyme, which results in altered ergosterol production and impaired cell membrane composition and permeability, which in turn leads to cation, phosphate, and low molecular weight protein leakage. In addition, miconazole inhibits fungal peroxidase and catalase while not affecting NADH oxidase activity, leading to increased production of reactive oxygen species (ROS). Increased intracellular ROS leads to downstream pleiotropic effects and eventual apoptosis. Lastly, likely as a result of lanosterol demethylation inhibition, miconazole causes a rise in intracellular levels of farnesol. This molecule participates in quorum sensing in _Candida_, preventing the transition from yeast to mycelial forms and thereby the formation of biofilms, which are more resistant to antibiotics. In addition, farnesol is an inhibitor of drug efflux ABC transporters, namely _Candida_ CaCdr1p and CaCdr2p, which may additionally contribute to increased effectiveness of azole drugs.

Pharmacodynamics

Miconazole is an azole antifungal that functions primarily through inhibition of a specific demethylase within the CYP450 complex. As miconazole is typically applied topically and is minimally absorbed into the systemic circulation following application, the majority of patient reactions are limited to hypersensitivity and cases of anaphylaxis. Patients using intravaginal miconazole products are advised not to rely on contraceptives to prevent pregnancy and sexually transmitted infections, as well as not to use tampons concurrently.

Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.

Molecular reference: triamcinolone

PubChem CID 31307

Molecular formula: C21H27FO6

Mechanism of action

Corticosteroids like triamcinolone inhibit phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes, which in turn prevent the formation of arachidonic acid, which decrease expression of cyclooxygenase and lipoxygenase, inhibiting synthesis of prostaglandins and leukotrienes. Anti-inflammatory activity occurs via reversal of vascular dilation and reducing permeability, which prevents macrophage and leukocyte migration. Triamcinolone also inhibits nuclear factor kappa-B, which decreases the production of pro-inflammatory signals such as interleukin-6, interleukin-8, and monocyte chemoattractant protein-1. Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/ Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocttes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. The overall actions of topical corticosteroids are catabolic. /Corticosteroids (topical)/ The potent anti-inflammatory action may be due to an inhibition of the secretion of growth factors, endothelial activating and other cytokines from lymphocytes, eosinophils, macrophages, fibroblasts, and mast cells. The results are decreased influx of inflammatory cells into the bronchial walls, due in part to inhibition of expression of adhesion molecules on the endothelium and in the tissue. Decreased activation and survival of eosinophils in the lung tissue and a reduction in numbers of mast cells are further effects. Corticosteroids may inhibit release of mediators from basophils and enzymes from macrophages. There is decreased permeability through vasoconstriction and direct inhibition of endothelial cell contradiction. Beta-adrenergic-receptor numbers may be increased, which results in an enhanced response to beta-adrenergic bronchodilators and reduced down-regulation of beta-receptors after prolonged beta-agonist exposure. Inhaled corticosteroids also inhibit mucus secretion in airways, possibly by a direct action on submucosal gland cells and an indirect inhibitory effect caused by the reduction in inflammatory mediators that stimulate mucus secretion. The amount and viscosity of sputum are reduced. /Corticosteroids (inhalation-local/

Pharmacodynamics

Triamcinolone is a corticosteroid with anti-inflammatory properties. These properties are used to treat inflammation in conditions that affect various organs and tissues. Triamcinolone should not be administered as an epidural injection.

Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.

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