1. Melasma
Is a common acquired hyperpigmentation of the skin, the etiology is associated with elements such as hormonal agents, genetics and ultraviolet radiation. Histologically, it is characterized by enhanced skin and/or dermal pigmentation and raised dermal veins, with an increased variety of pole cells at the website of the lesion.
System of Activity: Tranexa has pole cell activity-reducing, anti-angiogenic and also melanogenic residential properties.
2. Post-inflammatory hyperpigmentation
It is a sequela of reactive hyperpigmentation after skin inflammation or injury.
System of activity: Tranexa may lower the release of bradykinin by blocking plasmin, and may also inhibit the launch of leukotrienes and also platelet initiating elements by lowering the number and task of mast cells.
3. Acne-associated post-inflammatory erythema
It is a common sequela that takes place after acne swelling and also is connected with enhanced pro-inflammatory cytokines as well as neovascularization.
Mechanism of activity: Tranexa puts in anti-inflammatory impacts by lowering the expression of proinflammatory cytokines (interleukin 6 and also lump death factor α) and chemokines (CCL10).
4. Telangiectasia
Dilation of small blood vessels on the skin or mucous membrane surface area.
System of action: Tranexa hinders vascular endothelial growth factor-induced overexpression and also activation of vascular endothelial development element receptor in normal human melanocytes as well as human umbilical capillary endothelial cells, consequently preventing skin angiogenesis.
5. Riehl’s melanosis
It is a pigmented disordered skin disease, primarily manifested as gray-brown coloring on the face as well as neck.
System of activity: Tranexamic acid has a comparable chemical framework to tyrosine, which can directly take on tyrosine, interfere with the catalytic impact of tyrosinase on tyrosine metabolic rate, and reduce melanin manufacturing.
6. Rosacea
It is an usual chronic inflammatory skin disease of the face. The pathogenesis includes inherent immune irregularities, inflammatory response of the skin to microbes, ultraviolet light damages, as well as vascular hyperresponsiveness.
Device of action: Tranexa can boost the symptoms of rosacea by anti-inflammation, inhibiting angiogenesis, repairing the skin obstacle, and preventing the activation of protease-activated receptors by serine proteases.
7. Chronic urticaria
It refers to recurring urticaria with or without angioedema lasting for 6 weeks or more, and also its seriousness is connected to the generation of thrombin in plasma, fibrinolysis and also raised focus of inflammatory pens in plasma.
System of activity: Tranexa puts in anti-inflammatory impacts by minimizing the expression of pro-inflammatory cytokines and chemokines. Activation of plasmin turns on the kallikrein-kinin system, which mediates the release of bradykinin, which binds to B2 receptors in the subcutaneous as well as submucosal vasculature resulting in allergic reactions; tranexamic acid may act with Barring plasmin minimizes the release of bradykinin, as well as additionally hinders the launch of leukotrienes as well as platelet-activating factors by minimizing the number as well as activity of mast cells.
8. Angioedema
It is a self-limited local edema that occurs in subcutaneous or mucosal tissues, and its pathogenesis may be associated with mast cell degranulation, moderated by histamine or bradykinin.
9. All-natural skin aging and also photoaging
Device of activity: Tranexa boosts hyaluronic acid synthesis by increasing the variety of skin cells, prevents matrix metalloproteinases by obstructing plasmin, thus reducing the destruction of extracellular matrix in the dermis, and can decrease TNF-α, IL-6 and The degree of active oxygen particles to boost the natural aging of the skin. It is still in the stage of animal experiments, and also clinical tests have not yet been executed.
10. Reduce bleeding
As an antifibrinolytic drug, Tranexa reversibly binds to the lysine binding site on plasminogen, thereby avoiding its conversion into plasmin, inhibiting succeeding fibrinolysis, and also lastly achieving the objective of hemostasis.