⚜ Penetrates deep and remove the toughest of tan from the skin
⚜ Helps even out the skin tone and prevents the appearance of dark spots & pigmentation.
⚜ Treats tanning caused due to any reason like sun, pollution, etc.
⚜ Lightens existing blemishes, pigmentation and dark spots.
⚜ Heals acne and other scars
⚜ Repairs & rejuvenates dull skin by removing signs of fatigue from the face. Brightens the complexion, and combats dullness by reviving dull and tired skin
⚜ Reveals sensationally illuminating skin.
⚜ Removes the tanning from the skin without damaging the skin barrier
⚜ Enriched with antioxidants that protect cells from the damage caused by free radicals
⚜ Reduces Acne, White heads & Black heads
⚜ Tightens skin while making it supple and soft
⚜ Removes the dead tanned skin while deep cleansing the pores to reveal the healthy layer underneath
⚜ Helps in reproducing new cells, thus giving your skin a fresh and rejuvenated look
⚜ Repairs damage caused by sun and encourages even skin tone.
⚜ Stimulates collagen production and soothes and calms the skin
⚜ Locks in the necessary quantity of moisture, giving the facial skin the glow of youth
⚜ Smoothens skin texture and provides a relaxing and pampering spa experience at your own home

⚜ Use it weekly, as a self beauty care regimen at home.
⚜ Ideal for year round usage as its all season formula provides complete rejuvenation and detoxification

⚜ All skin types
⚜ For women and men.
⚜ Ideal for weekly rejuvenation and detoxification

Powders of Jojoba, Rosehip, Lemon Peel, Kinnu Peel, Spearmint, Fuller's Earth, Guava Leaf and Essential Oils of Ylang Ylang & Mandarin.

⚜ Store in a cool and dry place, away from direct sunlight.
⚜ For external use only.
⚜ Reading the ingredients list is recommended to ensure that the user is not allergic to any ingredient herb.
⚜ Patch test is recommended on a small area of the skin prior to first usage.

India

⚪ Tanning process
Melanin is a natural pigment produced by cells called melanocytes in a process called melanogenesis. Melanocytes produce two types of melanin: pheomelanin (red) and eumelanin (very dark brown). Melanin protects the body by absorbing ultraviolet radiation. Excessive UV radiation causes sunburn along with other direct and indirect DNA damage to the skin, and the body naturally combats and seeks to repair the damage and protect the skin by creating and releasing further melanin into the skin's cells. With the production of the melanin, the skin color darkens. The tanning process can be triggered by natural sunlight.
There are two different mechanisms involved in the production of a tan by UV exposure: Firstly, UVA radiation creates oxidative stress, which in turn oxidizes existing melanin and leads to rapid darkening of the melanin. UVA may also cause melanin to be redistributed (released from melanocytes where it is already stored), but its total quantity is unchanged. Skin darkening from UVA exposure does not lead to significantly increased production of melanin or protection against sunburn. In the second process, triggered primarily by UVB, there is an increase in production of melanin (melanogenesis), which is the body's reaction to direct DNA photodamage (formation of pyrimidine dimers) from UV radiation. Melanogenesis leads to delayed tanning, and typically becomes visible two or three days after exposure.The tan that is created by increased melanogenesis typically lasts for a few weeks or months, much longer than the tan that is caused by oxidation of existing melanin, and is also actually protective against UV skin damage and sunburn, rather than simply cosmetic. Typically, it can provide a modest Sun Protection Factor (SPF) of 3, meaning that tanned skin would tolerate up to 3 times the UV exposure as pale skin. However, in order to cause true melanogenesis-tanning by means of UV exposure, some direct DNA photodamage must first be produced, and this requires UVB exposure (as present in natural sunlight, or sunlamps that produce UVB). The ultraviolet frequencies responsible for tanning are often divided into the UVA and UVB ranges.
⚪ UVA
Ultraviolet A (UVA) radiation is in the wavelength range 320 to 400 nm. It is present more uniformly throughout the day, and throughout the year, than UVB. Most UVA is not blocked by the atmosphere's ozone layer. UVA causes the release of existing melanin from the melanocytes to combine with oxygen (oxidize) to create the actual tan color in the skin. UVA is blocked less than UVB by many sunscreens, but is blocked to some degree by clothing. UVA is known both to cause DNA damage and to be carcinogenic. However, it operates not by inducing direct DNA damage, but by producing reactive oxygen species which damage DNA indirectly. UVA induces a cosmetic tan but little extra melanin protection against sun damage, sun burn, or cancer.
⚪ UVB
Ultraviolet B (UVB) radiation is in the wavelength range 280 to 320 nm. Much of this band is blocked by the Earth's ozone layer, but some penetrates. UVB:
• triggers the formation of CPD-DNA damage (direct DNA damage), which in turn induces an increased melanin production.
• is more likely to cause a sunburn than UVA as a result of overexposure. The mechanism for sunburn and increased melanogenesis is identical.Both are caused by the direct DNA damage (formation of CPDs).
• produces Vitamin D in human skin.
• is reduced by virtually all sunscreens in accordance with their SPF.
• is thought to cause the formation of moles and some types of skin cancer.
• causes skin aging (but at a slower rate than UVA).
• stimulates the production of new melanin, which leads to an increase in the dark-colored pigment within a few days.

⚪ Mechanism of de-tanning action

De-tanning works by reducing the presence of melanin pigment in the skin. To accomplish this, there are several possible mechanisms of action:
• Inhibition of the activity of tyrosinase|Inhibition of the activity of tyrosinase: The catalytic action of tyrosinase is inhibited by the de-tanning agent.
• Inhibition of the expression or activation of tyrosinase: The anti melanogenic agent causes less tyrosinase to be generated or prevents tyrosinase from being activated to its functional form.
• Scavenging of the intermediate products of melanin synthesis.
• Preventing the transfer of melanosomes to keratinocytes

⚪ Inhibition of tyrosinase
Upregulation of tyrosinase caused by tyrosinase inhibitors. Several de-tanning agents, including tyrosinase inhibitors, have been found to cause an increase in the expression of tyrosinase, which by itself would increase melanin synthesis.
Microphthalmia-associated transcription factor (MITF) is the master transcription factor that controls the expression of TYR, TRP1, and TRP2, MART1, PMEL17, and many other important proteins involved in the function of melanocytes. Downregulation of MITF decreases melanogenesis and is a mechanism of action of some de-tanning agents. Various signaling pathways and genetic mutations influence the expression of MITF.
⚪ MC1R receptor and cAMP
The melanocortin 1 receptor (MC1R) is a transmembrane and G-protein coupled receptor expressed in melanocytes. MC1R is an important target for the regulation of melanogenesis. Agonism of MC1R increases the ratio of eumelanin to pheomelanin and increases the generation of melanin overall.
The MC1R and cAMP signaling pathway starts with the activation of MC1R, which causes activation of adenylyl cyclase (AC), which produces cyclic adenosine monophosphate (cAMP), which activates protein kinase A (PKA), which activates by protein phosphorylation cAMP response element-binding protein (CREB), which upregulates MITF, of which CREB is a transcription factor.
Alpha-melanocyte stimulating hormone (α-MSH), beta-melanocyte stimulating hormone (β-MSH), and adrenocorticotropic hormone are endogenous agonists of MC1R.[44]: 1175  Agouti signaling protein (ASIP) appears to be the only endogenous antagonist of MC1R. Synthetic MC1R agonists have been designed, such as the peptides afamelanotide and melanotan II.
⚪ Transfer of melanosomes
Within the skin, melanocytes are present in the basal layer of the epidermis; from these, melanocytes originate dendrites that reach keratinocytes.
Melanosomes, along with the melanin they contain, are transferred from melanocytes to keratinocytes when keratinocytes are low in the epidermis. Keratinocytes carry the melanosomes with them as they move toward the surface. Keratinocytes contribute to skin pigmentation by holding the melanin originating in melanocytes and inducing melanogenesis through chemical signals directed at melanocytes. The transfer of melanosomes to keratinocytes is a necessary condition for the visible pigmentation of the skin. Blocking this transfer is a mechanism of action of some de-tanning agents.
The protease-activated receptor 2 (PAR2) is a transmembrane and G-protein coupled receptor expressed in keratinocytes and involved in melanocyte transfer. Antagonists of PAR2 inhibit the transfer of melanosomes and have de-tanning effects, while agonists of PAR2 have the opposite effect.

⚜ Penetrates deep and remove the toughest of tan from the skin
⚜ Helps even out the skin tone and prevents the appearance of dark spots & pigmentation.
⚜ Treats tanning caused due to any reason like sun, pollution, etc.
⚜ Lightens existing blemishes, pigmentation and dark spots.
⚜ Heals acne and other scars
⚜ Repairs & rejuvenates dull skin by removing signs of fatigue from the face. Brightens the complexion, and combats dullness by reviving dull and tired skin
⚜ Reveals sensationally illuminating skin.
⚜ Removes the tanning from the skin without damaging the skin barrier
⚜ Enriched with antioxidants that protect cells from the damage caused by free radicals
⚜ Reduces Acne, White heads & Black heads
⚜ Tightens skin while making it supple and soft
⚜ Removes the dead tanned skin while deep cleansing the pores to reveal the healthy layer underneath
⚜ Helps in reproducing new cells, thus giving your skin a fresh and rejuvenated look
⚜ Repairs damage caused by sun and encourages even skin tone.
⚜ Stimulates collagen production and soothes and calms the skin
⚜ Locks in the necessary quantity of moisture, giving the facial skin the glow of youth
⚜ Smoothens skin texture and provides a relaxing and pampering spa experience at your own home

⚜ Use it weekly, as a self beauty care regimen at home.
⚜ Ideal for year round usage as its all season formula provides complete rejuvenation and detoxification

⚜ All skin types
⚜ For women and men.
⚜ Ideal for weekly rejuvenation and detoxification

Powders of Jojoba, Rosehip, Lemon Peel, Kinnu Peel, Spearmint, Fuller's Earth, Guava Leaf and Essential Oils of Ylang Ylang & Mandarin.

⚜ Store in a cool and dry place, away from direct sunlight.
⚜ For external use only.
⚜ Reading the ingredients list is recommended to ensure that the user is not allergic to any ingredient herb.
⚜ Patch test is recommended on a small area of the skin prior to first usage.

India

⚪ Tanning process
Melanin is a natural pigment produced by cells called melanocytes in a process called melanogenesis. Melanocytes produce two types of melanin: pheomelanin (red) and eumelanin (very dark brown). Melanin protects the body by absorbing ultraviolet radiation. Excessive UV radiation causes sunburn along with other direct and indirect DNA damage to the skin, and the body naturally combats and seeks to repair the damage and protect the skin by creating and releasing further melanin into the skin's cells. With the production of the melanin, the skin color darkens. The tanning process can be triggered by natural sunlight.
There are two different mechanisms involved in the production of a tan by UV exposure: Firstly, UVA radiation creates oxidative stress, which in turn oxidizes existing melanin and leads to rapid darkening of the melanin. UVA may also cause melanin to be redistributed (released from melanocytes where it is already stored), but its total quantity is unchanged. Skin darkening from UVA exposure does not lead to significantly increased production of melanin or protection against sunburn. In the second process, triggered primarily by UVB, there is an increase in production of melanin (melanogenesis), which is the body's reaction to direct DNA photodamage (formation of pyrimidine dimers) from UV radiation. Melanogenesis leads to delayed tanning, and typically becomes visible two or three days after exposure.The tan that is created by increased melanogenesis typically lasts for a few weeks or months, much longer than the tan that is caused by oxidation of existing melanin, and is also actually protective against UV skin damage and sunburn, rather than simply cosmetic. Typically, it can provide a modest Sun Protection Factor (SPF) of 3, meaning that tanned skin would tolerate up to 3 times the UV exposure as pale skin. However, in order to cause true melanogenesis-tanning by means of UV exposure, some direct DNA photodamage must first be produced, and this requires UVB exposure (as present in natural sunlight, or sunlamps that produce UVB). The ultraviolet frequencies responsible for tanning are often divided into the UVA and UVB ranges.
⚪ UVA
Ultraviolet A (UVA) radiation is in the wavelength range 320 to 400 nm. It is present more uniformly throughout the day, and throughout the year, than UVB. Most UVA is not blocked by the atmosphere's ozone layer. UVA causes the release of existing melanin from the melanocytes to combine with oxygen (oxidize) to create the actual tan color in the skin. UVA is blocked less than UVB by many sunscreens, but is blocked to some degree by clothing. UVA is known both to cause DNA damage and to be carcinogenic. However, it operates not by inducing direct DNA damage, but by producing reactive oxygen species which damage DNA indirectly. UVA induces a cosmetic tan but little extra melanin protection against sun damage, sun burn, or cancer.
⚪ UVB
Ultraviolet B (UVB) radiation is in the wavelength range 280 to 320 nm. Much of this band is blocked by the Earth's ozone layer, but some penetrates. UVB:
• triggers the formation of CPD-DNA damage (direct DNA damage), which in turn induces an increased melanin production.
• is more likely to cause a sunburn than UVA as a result of overexposure. The mechanism for sunburn and increased melanogenesis is identical.Both are caused by the direct DNA damage (formation of CPDs).
• produces Vitamin D in human skin.
• is reduced by virtually all sunscreens in accordance with their SPF.
• is thought to cause the formation of moles and some types of skin cancer.
• causes skin aging (but at a slower rate than UVA).
• stimulates the production of new melanin, which leads to an increase in the dark-colored pigment within a few days.

⚪ Mechanism of de-tanning action

De-tanning works by reducing the presence of melanin pigment in the skin. To accomplish this, there are several possible mechanisms of action:
• Inhibition of the activity of tyrosinase|Inhibition of the activity of tyrosinase: The catalytic action of tyrosinase is inhibited by the de-tanning agent.
• Inhibition of the expression or activation of tyrosinase: The anti melanogenic agent causes less tyrosinase to be generated or prevents tyrosinase from being activated to its functional form.
• Scavenging of the intermediate products of melanin synthesis.
• Preventing the transfer of melanosomes to keratinocytes

⚪ Inhibition of tyrosinase
Upregulation of tyrosinase caused by tyrosinase inhibitors. Several de-tanning agents, including tyrosinase inhibitors, have been found to cause an increase in the expression of tyrosinase, which by itself would increase melanin synthesis.
Microphthalmia-associated transcription factor (MITF) is the master transcription factor that controls the expression of TYR, TRP1, and TRP2, MART1, PMEL17, and many other important proteins involved in the function of melanocytes. Downregulation of MITF decreases melanogenesis and is a mechanism of action of some de-tanning agents. Various signaling pathways and genetic mutations influence the expression of MITF.
⚪ MC1R receptor and cAMP
The melanocortin 1 receptor (MC1R) is a transmembrane and G-protein coupled receptor expressed in melanocytes. MC1R is an important target for the regulation of melanogenesis. Agonism of MC1R increases the ratio of eumelanin to pheomelanin and increases the generation of melanin overall.
The MC1R and cAMP signaling pathway starts with the activation of MC1R, which causes activation of adenylyl cyclase (AC), which produces cyclic adenosine monophosphate (cAMP), which activates protein kinase A (PKA), which activates by protein phosphorylation cAMP response element-binding protein (CREB), which upregulates MITF, of which CREB is a transcription factor.
Alpha-melanocyte stimulating hormone (α-MSH), beta-melanocyte stimulating hormone (β-MSH), and adrenocorticotropic hormone are endogenous agonists of MC1R.[44]: 1175  Agouti signaling protein (ASIP) appears to be the only endogenous antagonist of MC1R. Synthetic MC1R agonists have been designed, such as the peptides afamelanotide and melanotan II.
⚪ Transfer of melanosomes
Within the skin, melanocytes are present in the basal layer of the epidermis; from these, melanocytes originate dendrites that reach keratinocytes.
Melanosomes, along with the melanin they contain, are transferred from melanocytes to keratinocytes when keratinocytes are low in the epidermis. Keratinocytes carry the melanosomes with them as they move toward the surface. Keratinocytes contribute to skin pigmentation by holding the melanin originating in melanocytes and inducing melanogenesis through chemical signals directed at melanocytes. The transfer of melanosomes to keratinocytes is a necessary condition for the visible pigmentation of the skin. Blocking this transfer is a mechanism of action of some de-tanning agents.
The protease-activated receptor 2 (PAR2) is a transmembrane and G-protein coupled receptor expressed in keratinocytes and involved in melanocyte transfer. Antagonists of PAR2 inhibit the transfer of melanosomes and have de-tanning effects, while agonists of PAR2 have the opposite effect.