Topical Curaderm cream is a cream that contains BEC glycoalkaloids that specifically seek out and destroy precancer and cancer cells without harming non-cancer cells.

Cancer cells have a mutant protein on their outer structure, normal non cancer cells do not contain this abnormal mutant protein known as RBP. Curaderm interacts and enters these cancer cells and kills them by an organized type of cell death, known as apoptosis that doesn’t result in scar formation. Normal cells are not affected by this procedure and are not killed.

Curaderm is indicated for actinic keratosis, basal cell carcinoma and intraepidermal carcinoma (in situ squamous cell carcinoma).

BEC the active ingredient in Curaderm is used to treat the following skin conditions:

• Psoriasis
• Sunscreen, that prevents skin cancer formation and also treats sunspots
• Curage, a range of skin care products to complement healing of the skin

Curaderm is a powerful medication and must be used exactly as directed.

Keep it in a secured area so other people cannot mistakenly use it to treat something else.

Curaderm is applied twice a day after washing with soap and plain water. A tiny amount of the cream should be gently applied to the visible lesions and covered with micropore dressing. Treatment periods depend on the type and size of the lesion, but should continue until healing occurs.

Curaderm cream frequently results in a mild to a severe stinging or burning sensation for several minutes, depending on the sensitivity of the skin and the severity of the lesion. Initially with Curaderm treatment, the lesion will appear to become bigger and after some time the lesion will reverse course and become smaller until it completely disappears.

Arrange for your health care professional to review you during treatment.

After you have completed the treatment, you may use the Curage moisturizer to speed-up the healing process. 

Skin cancer is the most common form of cancer. It most often develops on skin exposed to the sun. But this cancer also occurs on areas of the skin not directly exposed to sunlight. It occurs when there is an irregular growth of skin cells. There are three major types of skin cancer – basal cell carcinoma, squamous cell carcinoma and melanoma.

BCC begins in the basal cells, a cell layer at the bottom of the epidermis, the outermost layer of the skin, that produces new skin cells as old ones die off.  BCC occurs when a mutation occurs in the DNA of one or more basal cells.  The process of creating new skin cells is controlled by the basal cell’s DNA.  The DNA contains the instructions that tell the cell how to behave.  A mutation can tell the cell to multiply more rapidly and continue to grow when it would normally die.  For every normal cell, there is a time to live and a time to die.  Roughly 50 billion cells are born and die each day in humans. 

Under normal conditions, a programmed sequence of events, known as apoptosis, leads to the elimination of cells without releasing harmful substances into the surrounding area.  Basal cells in the basal cell layer (stratum basale) of the skin, is also referred to as basal keratinocytes.  Keratinocyte apoptosis plays a critical role in regulating epidermal development and restraining carcinogenesis. 

Apoptosis balances proliferation to maintain epidermal thickness and contributes to stratum corneum formation.  When basal cells are mutated, apoptosis may not work correctly, cells that should be eliminated may persist and become immortal, such as the case with BCC. 

BCC starts when basal cells grow out of control and crowd out normal cells.  In BCC, the process of apoptosis is defunct but cell division is intact resulting in excessive numbers of cancer cells, resulting in a change in the skin, such as a growth or a sore that will not heal. 

With BCC, these lesion changes in the skin may express one of the following characteristics:

• A pearly white, skin-coloured or pink bump that is translucent. Tiny blood vessels are often visible. BCC often appears on the face and ears.  The lesion may rupture, bleed and scab over.
• A flat, scaly, reddish patch with a raised edge often appears on the back or chest.
• A white, waxy, scar-like lesion without a clearly defined border, called morpheaform.
• A brown, blackish lesion with a slightly raised, translucent border.

Actinic keratosis (AK), also known as solar keratosis, is the most common pre cancer that forms on skin damaged by chronic exposure to ultraviolet (UV) rays from the sun and/or indoor tanning. AK is widespread, 58 million Americans have one or more AKs.

AKs often appear as small dry, scaly or crusty patches of skin, which may be red, white, pink, flesh toned, light or dark tan, or a combination of colours and are sometimes raised. Because of their rough texture, AK is often easier to feel than see.

AKs are found on the face, lips, ears, scalp, shoulders, neck, back of hands and forearms. Importantly, 5-10 percent of AKs turn into SCC.

Squamous cell carcinoma (SCC) of the skin is the second most common form of skin cancer.  SCC begins in the squamous cells that make up the middle and outer layers of the skin. SCC occurs when a mutation occurs in the DNA of one or more squamous cells. The DNA contains the instructions that tell the cell how to behave. A mutation can tell the cell to multiply more rapidly and continue to grow when it would normally die. For every normal cell, there is a time to live and a time to die. Roughly 50 billion cells are born and die each day in humans. Under normal conditions, a programmed sequence of events, known as apoptosis, leads to the elimination of cells without releasing harmful substances into the surrounding area. 

Mutation of the p53 gene results in inhibition of apoptosis of abnormal cells in all stages of SCC, starting at the precancerous lesion and advancing to the invasive and potentially metastatic forms. The pathogenesis of SCC is multifactorial consisting of extrinsic factors (such as UV sunlight exposure and industrial carcinogens) and intrinsic factors (such as age and immunosuppression).

Actinic keratosis is an initial observable precursor to SCC. Clinically, actinic keratoses are usually less than 1 cm, skin-coloured, red, brown, rough, sandpaper-like lesions. These precancerous lesions, if remain untreated, can continue to mutate and become SCC in situ. SCC in situ is a well-defined scaly plaque. Without treatment, SCC in situ can advance to form invasive SCC.

Invasive SCC invades into the dermis and may further invade fat, muscle, cartilage and bone. Metastasis to regional nodes with subsequent translocation to distant sites such as lungs and liver may then occur. SCC is composed of several variants, which are distinguishable, by histological assessment. 

Melanoma is a serious form of skin cancer that starts in cells known as melanocytes. A melanocyte is a specialized skin cell that produces the protective skin-darkening pigment melanin. Melanoma is more dangerous than other skin cancers because of its ability to spread to other organs more rapidly.

There are eight types of standard treatment: 

• Surgery
• Radiation therapy
• Chemotherapy 
• Photodynamic therapy
• Immunotherapy
• Targeted therapy
• Chemical peel
• Other drug therapy

Improving patient care and safety is of paramount importance to Curaderm Global.

Any medicines, no matter how safe and effective, can sometimes cause side effects.

Curaderm Global’s pharmacovigilance continuously evaluates information received from patients, healthcare professionals and members of the public ensuring the balance of benefits against risk