Radiaura Skin Recovery

RADIAURA SKIN RECOVERY- lidocaine hydrochloride and hydrocortisone acetate cream
PureTek Corporation

Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. For further information about unapproved drugs, click here.


Lidocaine HCI 3% — Hydrocortisone Acetate 0.5%

Anti-Inflammatory Anesthetic for Relief of Skin Inflammation

Radiaura Skin Recovery Cream was specifically formulated by well-known Radiation Oncologist Dr. Lauren Lukas MD. This unique formulation is indicated for relief of redness, pain, itching, and discoloration associated with inflammation and skin burns. For use after radiation treatment, cosmetic procedures, sun exposure, and for inflammatory skin conditions.

The main ingredients in Radiaura Skin Recovery Cream include lidocaine hydrochloride (HCl) 3% and hydrocortisone acetate 0.5%, as well as botanicals including curcumin (from turmeric), tetrahydrocurcumin (tetrahydrodiferuloylmethane, tetrahydrodemethoxydiferuloylmethane, tetrahydrobisdemethoxydiferuloylmethane — these are metabolites of curcumin from turmeric), boswellia serrata, copper-tripeptide, arbutin, calendula, camellia sinensis (green tea leaf extract), and cucumis sativus (cucumber extract). It also includes ChitoClear® chitosan which serves as a silicone substitute.


Lidocaine is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl), and has the following structure:

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Hydrocortisone acetate has a chemical name pregn-4-ene-3, 20-dione, 21-(acetyloxy)-11, 17-dihydroxy-(11β)-, It has the following structural formula:

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(click image for full-size original)

Radiaura Skin Recovery Cream Lidocaine HCl 3%- Hydrocortisone Acetate 0.5% Each gram contains Lidocaine HCl 30 mg, Hydrocortisone Acetate 5 mg.

Lidocaine HCl 3% (30 mg)

Hydrocortisone Acetate 0.5% (5 mg).


Aqua (Purified Water), Arbutin, Bis(Tripeptide-1) Copper Acetate, Bisabolol, Boswellia Serrata Extract, Brassica Campestris (Rapeseed) Sterols , Butyrospermum Parkii (Shea) Butter, Calendula Officinalis Flower Extract , Camellia Sinensis (Green Tea) Leaf Extract , Cannabis Sativa (Hemp) Seed Oil, Cetearyl Alcohol , Cetyl Alcohol , Chitosan, Coco-Caprylate/Caprate, Coconut Alkanes, Cucumis Sativus (Cucumber) Fruit Extract, Curcuma Longa (Turmeric) Root Extract, D- alpha-tocopherol, Dextrose, Glycerin, Glyceryl Stearate, Hydroxyethylcellulose, Jojoba Esters, Lecithin, PEG-100 Stearate, Phenoxyethanol, Polyglyceryl-3 Diisostearate, Simmondsia Chinensis (Jojoba) Seed Oil, Sodium Hyaluronate, Sodium Hydroxide, Sorbitan Stearate, Squalane, Stearic Acid, Stearyl Alcohol, Tetrahydrodiferuloylmethane, Tetrahydrodemethoxydiferuloylmethane, Tetrahydrobisdemethoxydiferuloylmethane



Product releases lidocaine to stabilize the neuronal membrane by inhibiting the ionic fluxes required for initiation and conduction of impulses, thereby effecting local anesthetic action. Hydrocortisone acetate provides relief of inflammatory and pruritic manifestations of corticosteroid responsive dermatoses.


Lidocaine may be absorbed following topical administration to mucous membranes, its rate and extent of absorption depending upon the specific site of application, duration of exposure, concentration, and total dosage. In general, the rate of absorption of local anesthetic agents following topical application occurs most rapidly after intratracheal administration. Lidocaine is also well-absorbed from the gastrointestinal tract, but little intact drug appears in the circulation because of biotransformation of the liver.
Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjungation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of lidocaine. Approximately 90% of lidocaine administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline.
The plasma binding of lidocaine is dependent of drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 g of free base per mL, 60 to 80 percent of lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid-glycoprotein.
Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.
Studies of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent is typically 1.5 to 2 hours. Because of the rapid rate at which lidocaine is metabolized, any condition that affects liver function may alter lidocaine kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites.
Factors such as acidosis and the use of CNS stimulants and depressants affect the CNS levels of lidocaine required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6 g free base per mL. In the rhesus monkey arterial blood levels of 18-21 g/mL have been shown to be the threshold for convulsive activity.
The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings.
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption. Occlusive dressings substantially increase the percutaneous absorption of topical corticosteroids. Thus, occlusive dressings may be a valuable therapeutic adjunct for treatment of resistant dermatoses.
Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Corticosteroids are bound to plasma protein in varying degrees. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.


The product is used for the anti-inflammatory and anesthetic relief of redness, pain, itching, and discoloration due to inflammation and skin burns. For the relief of redness, pain, itching, discoloration, inflammation and mild skin burns associated with radiation. For use after radiation treatment, cosmetic procedures, sun exposure, and for inflammatory skin conditions.


Product should not be used in patients with a history of sensitivity to any of its ingredients or adverse reactions to lidocaine or amide
anesthetics, which usually do not cross-react with “caine” ester type anesthetics. If excessive irritation and significant worsening occur, discontinue use and seek the advice of your physician. Product and topical lidocaine should be used cautiously in those with impaired liver function, as well as the very ill or very elderly and those with significant liver disease. Product should be used with caution in patients receiving antiarrhythmic drugs of Class I since the adverse effects are additive and generally synergistic. Product is contraindicated for tuberculous or fungal lesions or skin vaccinia, varicella and acute herpes simplex. Topical corticosteroids are contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation.

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