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Tetraacetylphytosphingosine (TAPS) is a sphingolipid metabolite produced by Wickerhamomyces ciferrii (also known as Hansenula ciferrii). It exerts an inhibitory action on angiogenesis through inhibition of the mitogen-activated protein kinase (MAPK) pathway and intracellular calcium increase. Therefore, TAPS was suggested as a potential treatment for angiogenesis related disorders such as arthritis, cancer and psoriasis.

Tetraacetylphytosphingosine(TAPS) is a modified form of phytoshingosine, which is a component found in the lipid layer of the skin and known for Moisturizing and Repairing the Skin. TAPS functions as a lipid source, contributing to the water-locking barrier of the skin's outer layer, the stratum corneum. This helps to increase the overall ceramide content in the skin, which is crucial for maintaining skin hydration and preventing dehydration by bolstering the skin's barrier function. Improving Dark Circles, TAPS has been found to inhibit the formation and leakage of capillaries. This action can be beneficial in improving the appearance of dark circles under the eyes. Promoting Skin Cell Regeneration and Repair, TAPS is also known to promote the regeneration and repair of skin cells. It stimulates the synthesis of critical structural proteins like collagen and elastic fibers, vital for maintaining skin elasticity and firmness.

Tetraacetylphytosphingosine was found to induce apoptosis in HaCaT human keratinocyte cells. In addition, it was demonstrated that TAPS synergistically increases UVB-induced apoptosis via caspase activation by regulating the level of pro-apoptotic Bax and anti-apoptotic Bcl-2 in HaCaT cells.

Tetraacetylphytosphingosine (TAPS; 5 μM; 24 h) markedly decreases VEGF-induced chemotactic migration and capillary-like tube formation in HUVEC. It significantly inhibits VEGF-induced proteolytic enzyme production, including MMP-2, urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1). It also suppresses VEGF-induced phosphorylation of p42/44 extracellular signal-regulated kinase and c-JNK. In addition, Tetraacetylphytosphingosine abolished VEGF-induced intracellular calcium increase. In HaCaT cells, Tetraacetylphytosphingosine co-treatment synergistically increases the level of UVB-induced apoptosis via caspase activation by regulating pro-apoptotic Bax and anti-apoptotic Bcl-2 levels.