DEFORAX cream contains aciclovir which used in treatment of different types of viral diseases like:

Herpes simplex virus–1 (HSV-1) which causes herpes labialis (cold sores).

Route of administration – Topical

Adults and children

DEFORAX Cream should be applied five times daily at approximately four hourly intervals, omitting the night time application. DEFORAX Cream should be applied to the lesions or impending lesions as soon as possible, preferably during the earliest stages (prodrome or erythema). Treatment can also be started during the later (papule or blister) stages. Treatment should be continued for at least 4 days. If healing has not occurred, treatment may be continued for up to 10 days. If lesions are still present after 10 days, users should be advised to consult a doctor. Users should wash their hands before and after applying the cream, and avoid unnecessary rubbing of the lesions or touching them with a towel, to avoid aggravating or transferring the infection.

• Only recommended for use on cold sores on the lips and face. 

• People with particularly severe Herpes labialis should be encouraged to seek medical advice. 

• Not to be applied to mucous membranes such as inside the mouth or vagina, or on the eye. Particular care should be taken to avoid contact with the eye. 

• Not for use for the treatment of genital herpes or ocular herpes infections. 

• Not recommended for use by patients who know they are immunocompromised e.g. by HIV infection, bone marrow transplant or cancer treatment, except on the advice of a doctor. 

• Cold sore sufferers should be advised to avoid transmitting the virus, particularly when active lesions are present.

Systemic administrated drugs are not likely interacting with topically applied acyclovir.

Probenecid increases the mean half-life and area under the plasma concentration curve of systemically administered aciclovir. Other drugs affecting renal physiology could potentially influence the pharmacokinetics of aciclovir.

The pregnancy risk factor for aciclovir is B. 

No specific studies of topical aciclovir have been carried out in pregnant women or nursing mothers. 

So far, no relevant plasma levels have been measured and no systemic effects have been observed. 

However, use of the cream should be considered only when the potential benefit outweighs the possibility of unknown risks. Foetal abnormalities were observed in non-standard tests in rats, but only following such high subcutaneous doses that maternal toxicity was produced. The clinical relevance of these findings is uncertain.

Following oral administration of 200 mg aciclovir five times a day, Aciclovir has been detected in breast milk at concentrations ranging from 0.6 to 4.1 times the corresponding plasma levels. These levels would potentially expose breast fed infants to Aciclovir doses of up to 0.3 mg/kg/day.

   Topical aciclovir shall not affect the ability to drive or use the machines.

Like all medicines, DEFORAX can cause side effects, although not everybody gets them.

The following convention has been used for the classification of undesirable effects in terms of frequency:- 

Very common 1/10, common 1/100 and <1/10, uncommon 1/1000 and <1/100, rare 1/10,000 and <1/1000, very rare <1/10,000. 

Skin and subcutaneous tissue disorders 

Common 

- Mild drying or flaking of the skin 

Uncommon 

- Itching 

Rare 

- Erythema 

- Contact dermatitis following application. Where sensitivity tests have been conducted, the reactive substances have most often been shown to be components of the cream base rather than aciclovir. 

Immune system disorders

Very rare 

- Immediate hypersensitivity reactions including angioedema. 

After application of the cream, transient burning or stinging of the treated skin areas may occur.

Call your physician or go to the nearest hospital emergency unit immediately.

Overdosage: application of 2gm DEFORAX cream topically is not expected to show undesirable effects.

Aciclovir is a pharmacologically inactive substance. After penetration into cells which are infected with herpes simplex virus types I and II (HSV I & HSV II) or varicella-zoster virus (VSV), Aciclovir is converted into a virostatic agent. The conversion of Aciclovir is catalysed by viral HSV- or VZV- thymidine kinase. Human thymidine kinase does not use Aciclovir effectively as a substrate; hence the toxicity to mammalian host cells is low.  

In the infected cell, Aciclovir is phosphorylated by viral thymidine kinase to Aciclovir monophosphate, which is further converted by cellular enzymes to Aciclovir triphosphate. Aciclovir triphosphate has a greater affinity for viral DNA polymerase than host cell DNA polymerase and therefore selectively interferes with the viral enzyme causing inhibition of viral DNA replication. Aciclovir is also incorporated into viral DNA by viral DNA polymerase, which results in chain termination, as Aciclovir lacks a 3'-hydroxyl group, preventing addition of nucleotides by 3', 5'-linkage. 

In several immunocompromised patients a longer or repeated treatment with Aciclovir can lead to a selection of viral strains with reduced sensitivity. As a result, these patients no longer respond to treatment with Aciclovir. Most of the clinical isolates with reduced sensitivity showed a relative lack of virus thymidine kinase. However, strains with changed/different virus thymidine kinase or DNA polymerase were also reported. The in vitro exposition of HSV-isolates can also lead to the development of less sensitive strains. The connection between the in vitro determined sensitivity of HSV-isolates and the clinical response to the treatment with Aciclovir is not clear.

Aciclovir penetrates into the skin. The intracutaneous concentration levels are higher than the minimal inhibitory concentration (MIC) in tissue at steady state. After topical application of Aciclovir, no Aciclovir plasma concentration could be determined. As the Aciclovir plasma concentrations following topical application are below the limit of detection, no pharmacokinetic studies are available on topical Aciclovir. Therefore, the following data is based on the data after oral or intravenous administration. Plasma protein binding is reported to range between 9% and 33% as a function of dose. The volume of distribution at steady state in adults is 50 ± 8.71ν1.73 m2, or 0.7 l/kg. Two metabolites could be identified in the urine of patients with normal renal function after single dosing with 14C-Aciclovir: 9-carboxymethoxymethylguanine (2%-14% of an administered dose) and 8-hydroxy-9-(2-hydroxyethoxymethyl) guanine (<0.2% of a dose). Subjects with normal renal function eliminate 62%-91% of an Aciclovir dose unchanged and 9%-14% as 9-carboxymethoxymethylguanine via the kidneys. Aciclovir is predominantly eliminated via the kidneys, preliminary by glomerular filtration and to a lesser extent by tubular secretion. 

In vitro and in vivo studies of Aciclovir cream and Aciclovir ointment versus oral Aciclovir were carried out to determine the bioavailability of Aciclovir in human skin. The in vitro studies used human skin biopsies, whilst the bioassays either used human skin grafts on mice or were carried out in the human eye (3 patients). The following dermal drug concentration gradient emerged for both topical and oral Aciclovir: stratum corneu > epidermi > dermis. There was no difference in concentration between cream and ointment. The upper layer of the epidermis on average showed a 48-fold higher concentration following topical application of Aciclovir ointment or cream 5% than after oral dosing, but the drug concentration in the basal epidermis – the site of herpes virus infection – was 2 to 3 times lower following topical application than after oral dosing. On the basis of continuous absorption the concentration increased as a function of time (higher drug concentrations being found 48 hours post-topical dose than 24 hours post-topical dose). Thus short dosing intervals appear rational for the special treatment of herpes simplex virus (HSV) infections.

For 24 days, PEG-based Aciclovir Cream 5% or 10% was applied to the shaved (intact and grazed) skin of guinea-pigs. The treated area corresponded to 10% of the body surface. There were neither systemic nor local toxic symptoms. This is also confirmed by histological studies and autopsy. According to the test carried out by Draize, who evaluated the allergic sensitising potential of a substance, there were no pathogenic findings. Studies carried out in swine showed that 5% Aciclovir cream in a PEG vehicle caused an only minimal (quantitative) delay in epidermal wound healing. Rabbits had 1%, 3% or 6% Aciclovir cream in a white petrolatum vehicle introduced directly into both eyes 5 times daily at 90-minute intervals for 3 weeks. Neither autopsy nor inspection nor histological examination revealed any pathological changes in the rabbit eyes.

   Not Applicable as it is topical product.

Do not store above 30°C.

To be used within one month after first opening.

Laminated polyfoil tube containing 5g or 10 g cream 

Collapsible aluminum tube containing 5g or 10 g cream​

Not all pack size marketed. 

Keep out of reach and sight of children.