Komfoderm K, cream 0.1% 30 g

Pharmacotherapeutic group:

Glucocorticosteroid for topical use

ATC code:

D07AA01

Pharmacological action

Pharmacodynamics

The active ingredient of Comfoderm® K, methylprednisolone aceponate, is a nonhalogenated synthetic steroid.

When applied topically, Comfoderm® K suppresses inflammatory and allergic skin reactions as well as reactions associated with increased proliferation, which results in reduction of objective symptoms of inflammation (erythema, edema, mottling) and subjective sensations (itching, irritation, pain, etc.).

When methylprednisolone aceponate is applied topically at the recommended dose, systemic effects are minimal in both humans and animals. After repeated application of methylprednisolone aceponate on large surfaces (40-60% of the skin surface), and also when used under the occlusive dressing no adrenal disturbances are noted: plasma cortisol level and its circadian rhythm remain within normal limits, there is no reduction of cortisol level in daily urine.

Methylprednisolone aceponate (especially its main metabolite, 6α-methylprednisolone-17-propionate) binds to intracellular glucocorticoid receptors. The steroid-receptor complex binds to specific DNA sites of immune response cells, thus causing a series of biological effects.

In particular, binding of the steroid-receptor complex to the DNA of the immune response cells leads to induction of macrocortin synthesis. Macrocortin inhibits the release of arachidonic acid and thus the formation of inflammatory mediators such as prostaglandins and leukotrienes. Inhibition by glucocorticosteroids of the synthesis of vasodilatory prostaglandins and potentiation of the vasoconstrictor effect of adrenaline, lead to a vasoconstrictor effect.

Pharmacokinetics

In external use methylprednisolone aceponate is hydrolyzed in the epidermis and dermis.
The main and most active metabolite is 6α-methylprednisolone-17-propionate, which has a significantly higher affinity for glucocorticosteroid receptors in the skin, indicating the presence of its “bioactivation” in the skin.

The extent of percutaneous absorption depends on the skin condition and the route of application (with or without an occlusive dressing). Percutaneous absorption in children and adults with atopic dermatitis (neurodermatitis) and psoriasis is less than 2.5%, which is only slightly higher compared to healthy volunteers (0.5-1.5%).

After entering the systemic bloodstream 6α-methylprednisolone-17-propionate rapidly conjugates with glucoronic acid, and thus in the form of 6α-methylprednisolone-17-propionate glucuronide is inactivated.
Metabolites of methylprednisolone aceponate are eliminated mainly by kidneys with the elimination half-life of about 16 hours. Methylprednisolone aceponate and its metabolites do not cumulate in the body.

Indications

Inflammatory skin diseases sensitive to therapy with topical glucocorticosteroids:

atopic dermatitis, neurodermatitis, childhood eczema;
true eczema;
microbial eczema;
simple contact dermatitis;
allergic (contact) dermatitis;
dyshidrotic eczema.

Pharmacological effect

Pharmacotherapeutic group:

glucocorticosteroid for local use

ATX code:

D07AA01

Pharmacological action

Pharmacodynamics

The active component of Comfoderm® K, methylprednisolone aceponate, is a non-halogenated synthetic steroid.

When applied externally, Comfoderm® K suppresses inflammatory and allergic skin reactions, as well as reactions associated with increased proliferation, which leads to a reduction in objective symptoms of inflammation (erythema, swelling, weeping) and subjective sensations (itching, irritation, pain, etc.).

When methylprednisolone aceponate is used topically at the recommended dose, the systemic effect is minimal in both humans and animals. After repeated application of methylprednisolone aceponate to large surfaces (40-60% of the skin surface), as well as when applied under an occlusive dressing, no dysfunction of the adrenal glands is observed: the level of cortisol in plasma and its circadian rhythm remain within normal limits, and there is no decrease in the level of cortisol in daily urine.

Methylprednisolone aceponate (especially its main metabolite, 6α-methylprednisolone-17-propionate) binds to intracellular glucocorticoid receptors. The steroid receptor complex binds to specific regions of the DNA of immune response cells, thereby causing a series of biological effects.

In particular, the binding of the steroid receptor complex to DNA by immune response cells leads to the induction of macrocortin synthesis. Macrocortin inhibits the release of arachidonic acid and, thereby, the formation of inflammatory mediators such as prostaglandins and leukotrienes. Inhibition of the synthesis of vasodilating prostaglandins by glucocorticosteroids and potentiation of the vasoconstrictor effect of adrenaline lead to a vasoconstrictor effect.

Pharmacokinetics

When applied externally, methylprednisolone aceponate is hydrolyzed in the epidermis and dermis.
The main and most active metabolite is 6α-methylprednisolone-17-propionate, which has a significantly higher affinity for glucocorticosteroid receptors of the skin, which indicates the presence of its “bioactivation” in the skin.

The degree of percutaneous absorption depends on the condition of the skin and the method of application (with or without an occlusive dressing). Percutaneous absorption in children and adults with atopic dermatitis (neurodermatitis) and psoriasis is no more than 2.5%, which is only slightly higher compared to healthy volunteers (0.5-1.5%).

After entering the systemic circulation, 6α-methylprednisolone-17-propionate quickly conjugates with glucuronic acid and is thus inactivated in the form of 6α-methylprednisolone-17-propionate glucuronide.
Metabolites of methylprednisolone aceponate are eliminated mainly by the kidneys with a half-life of about 16 hours. Methylprednisolone aceponate and its metabolites do not accumulate in the body.

Special instructions

In the presence of bacterial dermatoses and/or dermatomycosis, in addition to therapy with Comfoderm® K, it is necessary to carry out specific antibacterial or antimycotic treatment.

The drug is not intended for use in ophthalmology. Contact with eyes and mucous membranes should be avoided. As with the use of systemic corticosteroids, glaucoma may develop after external use of glucocorticoids (for example, when using the drug in high doses, due to very long-term use of occlusive dressings or application to the skin around the eyes).

Impact on the ability to drive vehicles and operate machinery

Not identified.

Active ingredient

Methylprednisolone aceponate

Composition

100 g of cream contains:

Active substance: methylprednisolone aceponate in terms of 100% substance – 0.10 g;

Excipients: ceramides – 0.50 g, preservative Euxyl PE 9010 (phenorxyethanol – 90%, ethylhexylglycerol 10%) in terms of phenoxyethanol – 0.90 g, isopropyl myristate – 7.00 g, octyldodecanol – 7.00 g, hexyldecyl stearate – 7.00 g, dimethicone 100 cst – 1.00 g, propylene glycol – 7.00 g, macrogol 40 stearate – 1.50 g, glyceryl monostearate – 8.50 g, cetostearyl alcohol (cetyl alcohol 60%, stearyl alcohol 40%) – 2.0 g, disodium edetate – 0.10 g, potassium dihydrogen phosphate – 0.49 g, sodium hydrogen phosphate dodecahydrate – 0.01 g, purified water – up to 100 g.

Pregnancy

If it is necessary to use Comfoderm® K during pregnancy and breastfeeding, the potential risk to the fetus and the expected benefits of treatment for the mother should be carefully weighed. During these periods, long-term use of the drug on large areas of the skin is not recommended.
Nursing mothers should not apply the drug to the mammary glands.

Contraindications

Hypersensitivity to the components of the drug;
tuberculous or syphilitic processes in the area of ​​​​application of the drug;
viral diseases (for example, chicken pox, herpes zoster) in the area where the drug is applied;
rosacea, perioral dermatitis in the area of ​​application of the drug;
areas of skin with manifestations of a reaction to vaccination;
children up to 4 months old

Side Effects

The incidence of side effects is classified according to the recommendations of the World Health Organization (WHO): very common (≥10%), common (≥1%, <10%), uncommon (≥0.1%, <1%), rare (≥0.01%, <0.1%), very rare (<0.01%), frequency unknown (it is not possible to estimate the frequency).Disorders of the skin and subcutaneous tissues: rarely – perioral dermatitis, skin depigmentation, allergic reactions to the components of the drug; frequency unknown – skin atrophy, telangiectasia, striae, acne-like skin changes (when using the drug for more than 4 weeks and/or on an area of ​​10% or more of the body surface).General disorders and disorders at the injection site: rarely – folliculitis, hypertrichosis; very rarely – itching, burning, erythema, formation of a vesicular rash; frequency unknown – systemic effects due to absorption.
If any of the side effects indicated in the instructions worsen, or any other side effects not listed in the instructions are noted, you should immediately inform your doctor.

Interaction

Not studied.

Overdose

When studying the acute toxicity of methylprednisolone aceponate, no risk of acute intoxication was identified from excessive single dermal use (application of the drug over a large area under conditions favorable for absorption) or from unintentional ingestion.

Symptoms: with excessively long and/or intensive external use of GCS, skin atrophy (thinning of the skin, telangiectasia, striae) may develop.

Treatment: if signs of skin atrophy appear, the drug must be discontinued.

Functional features

Suction and distribution

The extent of percutaneous absorption depends on the condition of the skin and the method of application (with or without an occlusive dressing). Percutaneous absorption in children and adults with atopic dermatitis (neurodermatitis) and psoriasis is no more than 2.5%, which is only slightly higher compared to healthy volunteers (0.5-1.5%). After entering the systemic circulation, 6α-methylprednisolone-17-propionate quickly conjugates with glucuronic acid and is thus inactivated in the form of 6α-methylprednisolone-17-propionate glucuronide.

Methylprednisolone aceponate and its metabolites do not accumulate in the body.

Metabolism and excretion

When applied externally, methylprednisolone aceponate is hydrolyzed in the epidermis and dermis. The main and most active metabolite is 6α-methylprednisolone-17-propionate, which has a significantly higher affinity for glucocorticoid receptors in the skin, indicating the presence of its “bioactivation” in the skin.

Metabolites of methylprednisolone aceponate are eliminated mainly by the kidneys with a T1/2 of about 16 hours.

Storage conditions

The drug should be stored out of the reach of children at a temperature not exceeding 25°C.

Shelf life

2 years.

Do not use after expiration date.

Manufacturer

Akrikhin JSC, Russia