Skin "Armor Guardian" | Recombinant humanized filaggrin
Filaggrin (FLG) is an important component of the stratum corneum and an important molecule that connects keratin fibers in the stratum corneum of human skin. It is distributed in different parts of the stratum corneum and is gradually degraded by enzymes during the migration of keratinocytes. It is degraded into small molecules such as natural moisturizing factors required by the stratum corneum and plays an important role in moisturizing and barrier integrity. The precursor of filaggrin, pro-filagrin, is distributed in the granular layer, while filaggrin is wrapped around the outside of keratinocytes in the form of a cornified membrane and also exists inside keratinocytes. With the help of filaggrin monomers, keratin fibers gather regularly and form a solid physical barrier in the outermost layer of the epidermis, which can prevent the loss of epidermal moisture and the invasion of external allergic substances.
Recombinant humanized filaggrin
Natural moisturizing factor, strong repair and moisturizing
Moisturizing / repair
The health and vitality of the skin cannot be separated from the expression of filaggrin. The important role of filaggrin (FLG) in the skin system is like putting on a "protective coat" for the skin.
When the skin is dry, it is easily irritated by various substances and causes allergies. As a wall to protect the inside, the skin has its own barrier function. This barrier function is that the internal substances cannot go to the outside, and the external things cannot enter the skin. This substance that can prevent the internal things from going out contains a component called keratin, and filaggrin is a kind of skin protein that promotes the coagulation of keratin and is then degraded into natural moisturizing factor. Natural moisturizing factor is a general term for the moisturizing components that the skin itself has. If the natural moisturizing factor decreases, the moisturizing function will decrease and it will become dry easily. Therefore, filaggrin plays a key role in the skin barrier function.
Among patients with atopic dermatitis, one in every three to four people is unable to produce filaggrin normally or produces less filaggrin. The causes of atopic dermatitis vary, not only because of the low production of filaggrin, but also because of sweat irritation or staphylococcus on the skin surface. However, if the skin cannot produce enough filaggrin, the skin's moisturizing and resistance will be weakened.
In 2006, a major discovery revealed that the cause of diseases such as ichthyosis and atopic dermatitis (AD) is the complete loss of the filaggrin gene, which leads to the destruction of the skin barrier.
The British Journal of Dermatology reported in 2013 that the mutation rates in Europeans and Asians were 7.7% (range 2.7-14.2) and 3.0% (range 0-7.3) respectively.
The 2019 Filaggrin and atopic march pointed out that the mutation frequency of filaggrin in the general population is 8-10%.
To date, approximately 60 loss-of-function filaggrin mutations have been identified, and the most common mutations in European populations are R501X and 2282del4, which lead to premature transcription or inappropriate processing of profilaggrin in filaggrin, thereby damaging the skin barrier structure and causing skin inflammatory responses.
The lack of FLG can cause a series of skin barrier-related problems or diseases
Studies have shown that the lack of FLG can lead to a fragile skin barrier, which in turn leads to increased stimulation of the skin by exogenous factors, triggering a series of skin allergies and inflammatory reactions, and further weakening the skin barrier
