SkinCeuticals Phloretin CF Serum

Product Information

Skinceuticals CE Ferulic and Phloretin CF are the two most popular Vitamin C serums from the brand. How do they compare? Phloretin CF provides powerful antioxidant protection, suitable for Normal, Oily and Combination skin types to improve discolouration, fine lines and wrinkles with its blend of phloretin, vitamin C and ferulic acid. If you’re serious about antiaging, you need this baby in your skincare routine. But be careful! L-Ascorbic Acid has a couple of side effects you should be aware of:

Anti-inflammatory effect of phloretin through inhibition of phosphorylation of MAPKs and IκBα. Most of the studies on the activation of inflammatory mediators from immune cells employed LPS which interacts with its receptor, TLR4. While a direct effect on TLR1/2 has been suggested, most of the data indicate an inhibitory effect on NF-κB mobilization to the nucleus. The LPS response shown by blue arrows includes the degradation of the NF-κB inhibitory protein, IκBα, via promoting its phosphorylation. This frees the p65/p50 to mobilise to the nucleus and activate inflammatory target genes such as COX, iNOS, and cytokines including TNF-α, IL-1β, and IL-6. Phloretin has been shown the suppress the NF-κB activity by inhibiting IκBα degradation (see red lines). The exact mechanism of how the MAPK activity leads to the activation of proinflammatory genes has not yet been fully established but the key steps after induction by inflammatory agents such as LPS is the phosphorylation of p38, ERK, and JNK which have been shown to be targeted by phloretin (see red lines). Note that other pro-inflammatory agents such as TNF-α, IL-1β, and IL-6 can also activate the MAPK and NF-κB pathways by interacting with their cell-surface receptors.Irritation:High concentrations (%15) of L-Ascorbic Acid – especially at the low pH (below 3) it needs to work its magic – can irritate skin, especially if it’s sensitive. Phloretin CF uses 10%, a concentration that’s sensitive skin-friendly. Due to air and light exposure, vitamin C products can darken after opening. The formula will remain effective. No, Skinceuticals isn’t cruelty-free. They may test on animals or outsource the process. Their parent company, L’Oreal, surely does. Price & Availability NOTE: The colours indicate the effectiveness of an ingredient. It is ILLEGAL to put toxic and harmful ingredients in skincare products. Helps prevent free radical damage, diminishes the appearance of discolouration and improves skin tone and texture.

SkinCeuticals Phloretin CF contains three potent antioxidants that can help to protect your skin from free radical damage while also promoting a more youthful complexion. While C E Ferulic is the ideal topical antioxidant for fine lines, wrinkles, loss of firmness and skin brightening in normal, dry and sensitive skin types, Phloretin CF may be a better choice for normal, oily and combination skin experiencing discoloration along with visible signs of aging. Both topical antioxidants feature L-ascorbic acid (the purest form of vitamin C) and ferulic acid, but the addition of phloretin is what makes Phloretin CF unique. In other words, for me, Skinceuticals CE Ferulic wins hands down in every respect. But hey, if you’re curious to try Phloretin, you’ll still get a few antioxidant benefits. How Does Skinceuticals Phloretin CF Compare To The Other Skinceuticals Vitamin C Serums? Experienced retinol users generally tolerate a higher concentration. Once your skin is comfortable with Retinol 0.3, you may step up to Retinol 0.5. This concentration can also be used by first-timers with resistant skin that rarely experiences irritation. Pure vitamin C (l-ascorbic acid): lauded for its superior antioxidant benefits, this highly potent form of pure vitamin C neutralizes damaging free radicals and protects against oxidative stress while providing visible anti-aging benefits.Hi, I'm Gio. I'm a no-nonsense, tell-it-like-it-is skin coach and writer on a mission to help you achieve your best skin day ever - every day. I bust skincare myths and debunk marketing jargon to help you figure out what's worth the splurge and what's best left on the shelf - using science, not hype. I also offer skincare consultations to help you create the best skincare routine for your unique needs. In a diabetic neuropathy study induced by STZ, phloretin (50 or 25 mg/kg, i.p.) or in combination with duloxetine (15 mg/kg duloxetine and 25 mg/kg phloretin, i.p.) was shown to ameliorate the thermally induced hyperalgesia, sciatic nerve oxidative stress markers (tissue MDA, NO, SOD activity and GSH levels); and sciatic nerve TNF-α and IL-6 levels [ 107]. This, together with the normalization of histopathological and structural changes, suggests the potential of phloretin as a neuroprotective agent. In HFD- and STZ-induced diabetes models in mice, phlorizin (10–20 mg/kg, p.o.) was shown to alleviate depression symptoms, reversed the decline in GSH, BDNF, and its receptor (TrkB), cyclic AMP-responsive element-binding protein (CREB) and ERK level [ 108]. Inflammatory markers were not, however, assessed in this study. Green: It’s effective, proven to work, and helps the product do the best possible job for your skin. Another way that ascorbic acid helps to reduce signs of aging is through collagen synthesis. Specifically, ascorbic acid serves as a cofactor for prolysyl and lysyl hydroxylase, the enzymes that are responsible for stabilizing and cross-linking the collagen molecules. Thus, SkinCeuticals Phloretin CF may be able to help reduce the appearance of fine lines and wrinkles while promoting firmer, more youthful skin.

The best vitamin C serums have the power to promote the skin’s collagen and elastin production, neutralise free radicals from environmental stress, and brighten the complexion – helping to fade and prevent hyperpigmentation. Vitamin C – the ingredient also known as ascorbic acid or l-ascorbic acid – really is an anti-ageing powerhouse, but not all skincare formulas centred on the antioxidant are made equal. Phloretin: Derived from apples and the root bark of fruit trees including apple, pear, and grapefruit, this antioxidant neutralizes damaging free radicals, helps improve cell turnover, and improves the appearance of discoloration I’ve already told you how Skinceuticals Phloretin CF compares to Skinceuticals CE Ferulic. To me, the latter is the BEST Vitamin C serum on the market (and yes, it makes me cry, it’s so expensive!), so I don’t see the need for more Vitamin C serums. Skinceuticals obviously disagrees with me as they have quite a few options available. Let’s take a look at how Skinceuticals Phloretin CF compares to them: One common link to the release of the above-mentioned proinflammatory mediators from activated macrophages is the nuclear transcription factor κ-B (NF-κB) which regulates the expression of several genes (e.g., chemokines, cytokines, and adhesion molecules) involved in inflammation. For details of NF-κB signalling, readers can refer to the numerous review articles in the field (e.g., [ 40, 41]). The NF-κB represents a family of protein transcription factors such as NF-κB1 (also named p50), NF-κB2 (also named p52), RelA (also named p65), RelB, and c-Rel. The expression of target genes happens when these transcription factors translocate from the cytoplasm to the nucleus and bind (through their transcriptional transactivation domain at their C-terminus) to the κB enhancer region of the DNA. Since the NF-κB proteins are sequestered in the cytoplasm by binding to inhibitory proteins, including inhibitors of κB (IκB) family members (most important is IκBα, others include IκBβ, IκBε, and their precursors), releasing the NF-κB from the complex is a key cell signalling step in inflammatory genes activation. Many agents that activate the inflammatory pathway such as LPS stimulate the degradation of IκBα via the multi-subunit IκB kinase (IKK)-induced phosphorylation. This further triggers ubiquitin-dependent IκBα degradation in the proteasome, thereby allowing the nuclear translocation of NF-κB. The IKK itself is a complex of two kinases (IKKα and IKKβ) and other proteins and constitutes the classic example of the canonical NF-κB pathway of activation which is common to various immunostimulant-based macrophage activation: i.e., the IκBα degradation-execute the canonical activation pathway of NF-κB. A variety of inflammatory stimuli activate the canonical pathway in macrophages, and these include proinflammatory cytokines, pattern-associated molecular patterns (PAMPs), or damage-associated molecular patterns (DAMPs) binding to cognate receptors. The LPS is recognised in macrophages by Toll-like receptors (e.g., TLR4) and its stimulatory effect is orchestrated through the canonical pathway. Other pathways or the noncanonical NF-κB pathway of activation are, however, also known. Activation of macrophages to a phenotypically M1 state leads to the induction of inflammatory mediators (e.g., IL-1, IL-6, IL-12, TNF-α, and chemokines) which promotes the process of inflammation while the M2 phenotype leads to the production of anti-inflammatory cytokines (e.g., IL-10 and IL-13) which promote resolution of inflammation (e.g., during the wound healing stage) [ 42]. Most of the anti-inflammatory mechanisms of phloretin discussed in the following sections are associated with modulation of the above-mentioned signalling pathway of NF-κB including macrophage polarisation. But I love fragrance-free products. Fragrance is one of the most (if not the most) irritating ingredient in skincare products. By taking it out, you greatly lower the risk someone will have an allergic reaction to it.SkinCeuticals Phloretin CF is an advanced daytime antioxidant serum that provides superior environmental protection that is a pigment regulator helping to reduce dullness and discolouration of the skin, it retextures and evens skin tone for a brighter more radiant complexion. Suitable for normal, combination skin with ageing and hyperpigmentation. One: it removes everything that’s not absolutely necessary, like fragrance and fancy plant extracts that look good in the marketing copy but do absolutely nothing for your skin. Instead, you have to trust the science here. Vitamin C + Phloretin + Ferulic Acid can protect your skin from environmental damage so that it ages slowly – but it takes years to see results.

A final way that ascorbic acid can improve the appearance of your skin is through its ability to reduce the appearance of dark spots and correct uneven skin tone. This is accomplished through inhibition of melanin synthesis. Melanin is a pigment that gives our skin color, but too much of this pigment can lead to undesirable dark spots called hyperpigmentation. Ascorbic acid decreases melanin formation by inhibiting tyrosinase, an enzyme that is required for melanin synthesis. Thus, SkinCeuticals Phloretin CF can help the skin to appear brighter with less dark spots and a more even skin tone. In the morning, after cleanser and before sunscreen to boost its sun protection. You could potentially use it in the evening as well, but I prefer to alternate my actives and use Vitamin C in the morning and retinol or an exfoliant at night. The most common skin concern during pregnancy is hyperpigmenation. According to the British Association of Dermatologists, it can affect up to 50% of women during their pregnancy, because hormones are slightly out of kilter and your body starts to produce more oestrogen. Combined with an increase in photosensitivity, this presents itself as large patches of discolouration on the face. The increase in oestrogen is also why your areola (the round area around your nipples) darkens. Evidence is now emerging in support of the PI3K/Akt pathway of NF-κB activation which is targeted by phloretin. Readers should bear in mind that this pathway is far too complex and in some cases, inhibition of the pathway displays protective effects while in others, it worsens the inflammation (see review, [ 121]). More research is thus needed to ascertain the significance of either enhancing or suppressing the PI3K/Akt pathway by phloretin.A considerable level of research has been done in the past few years to show that the antioxidant and anti-inflammatory effects of several compounds are mediated through the expression of the Nrf2, which derives macrophage to anti-inflammatory phenotype (M2). The Nrf2 is another master transcription factorthat regulates the cellular response to inflammationand oxidative stress. The Nrf2 binds to the regulatory regions (antioxidant response element (ARE)) of target genes to upregulate the expression of cytoprotective or antioxidant enzymes such as phase II detoxification enzymes and stress proteins. By far the most characterised genes/proteins under the regulatory control of Nrf2 are haeme oxygenase-1 (HMOX1, HO-1), glutamate-cysteine ligase, glutathione peroxidase 1 (GPX1), thioredoxin reductase 1 (Txnrd1), NAD(P)H-quinone oxidoreductase 1 (NQO1), glutathione- S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), peroxiredoxin (PRDX1), and ferritin. The Nrf2 activity depends on the negative regulator, Kelch-like ECH-associated protein 1 (Keap1, also called electrophile response element), which binds to it and presents it for ubiquitination and subsequent degradation by proteosomes. External stimuli such as ROS-based electrophilic reaction with Keap1 lead to the inactivation of Keap1 and leave the Nrf2 stable or available for nuclear translocation, and transcriptional induction of Nrf2-target genes. Alternative mechanisms of Nrf2 regulation are also known but not discussed herein. For details of Nrf2 regulation in inflammation/oxidative stress, readers should refer to review articles on this topic [ 56, 57, 58, 59]. In this line, phloretin (50 μM) treatment of mouse bone marrow-derived macrophages have been shown to reduce the inflammatory phenotype of macrophages through the upregulation of the Nrf2-signalling pathway [ 33]. In macrophages stimulated with phorbol 12-myristate 13-acetate, the levels of ROS and mRNA of proinflammatory genes NOS2, IL-6, COX2,and IL-12 were all shown to be reduced by phloretin, while Nrf2-response genes, HO-1and NQO1were activated. Interestingly, Keap1 degradation in macrophages was enhanced by phloretin. Furthermore, phloretin treatment led to the AMP-activated protein kinase (AMPK) phosphorylation and activation in macrophages which was shown to be associated with cell autophagy (see details in Section 12). In an in vivo model, a macrophage-driven experimental autoimmune encephalomyelitis (EAE) was reported to be suppressed by phloretin (50 mg/kg, i.p.). This was evidenced by increased expression of anti-inflammatory and neurotrophic factors, i.e., IL-4, ciliary neurotrophic factor, and insulin-like growth factor-1 in the spinal cord of EAE animals, elevated Nrf2 signalling in the CNS and increased mRNA expression of Nrf2 and its downstream targets, NQO1 and GPX1. The anti-inflammatory potential of phloretin was assessed both in vitro and in vivo using an experimental model of airway inflammation induced by cigarette smoke [ 82]. When the human lung mucoepidermoid cells (NCI-H292 cell line) were exposed to cigarette smoke extract (CSE), the expression of mucin 5ac (MUC5AC) and IL-1β were greatly enhanced, and phloretin suppressed this induction in a dose-dependent manner (1–5 µM). The CSE-induced phosphorylation of epidermal growth factor receptor (EGFR), ERK, and P38 was also inhibited by phloretin. In mice treated with phloretin (10 or 20 mg/kg, i.p.), the effect of CSE in lung histological changes, mucus hypersecretion, MUC5AC expression level, inflammatory cell infiltration in the lungs, and phosphorylation of EGFR, ERK, and P38 were suppressed. Respiratory pathogens ( Haemophilus influenzae) induced chronic obstructive pulmonary disease (COPD) in mice could also be suppressed by phloretin (0.157% in a diet for a week) as evidenced by reduced bacterial burden, inflammatory score in the lungs, and expression of a neutrophil chemoattractant, chemokine (C-X-C motif) ligand 1 (CXCL1) [ 44]. In this study [ 82], the pathogen-induced mucin production was also suppressed by phloretin. In RAW 264.7 macrophages exposed to COPD associated pathogens ( Moraxella catarrhalis and Streptococcus pneumoniae) and nontypeable Haemophilus influenzae (NTHi)-induced human bronchial epithelial (HBE) cells, the enhanced TNF secretion was suppressed by phloretin (100 µM) [ 44]. The direct effect of phloretin on bacteria should not also rule out as a mechanism contributing to the inhibition of pathogenic bacteria-induced lung inflammation. For example, human alveolar epithelial cell (A549 cells) damage caused by S. aureus in vitro could be ameliorated by phloretin (2–16 µg/mL) perhaps through a mechanism including a direct effect on bacteria such as an effect on the activity of the virulence factors, as shown for sortase B [ 82].