Pillar Guide · Skincare Science
Tranexamic acid for skin: dark spots, melasma, and what alpha arbutin adds to the picture
Tranexamic acid for skin works by blocking the UV-triggered signaling cascade that tells melanocytes to overproduce pigment, not by scrubbing pigment away. Clinical trials show topical concentrations of 2% to 5% support a significant reduction in melasma severity scores within 8 to 12 weeks. Alpha arbutin, which directly inhibits the tyrosinase enzyme downstream, pairs naturally with it to address two separate points in the pigmentation pathway.
Dark spots are a surface symptom of a deeper signaling problem. Ultraviolet exposure, inflammation, and hormonal shifts all trigger a chemical conversation between keratinocytes and melanocytes that ends with excess melanin. Tranexamic acid (TXA) interrupts that conversation early. Alpha arbutin blocks the enzyme that converts the signal into pigment. Understanding the mechanism is what separates actives that actually work from ones that just sound plausible.
// What's in this guide
- What is tranexamic acid, and where does it come from?
- How tranexamic acid works on skin pigmentation
- The clinical evidence: what the trials actually show
- Alpha arbutin: mechanism and why it complements TXA
- Brightening actives compared: an informational table
- How to use tranexamic acid and alpha arbutin together
- Skin tone and type considerations
- FAQ
01What is tranexamic acid, and where does it come from?
Tranexamic acid is a synthetic derivative of the amino acid lysine. It was developed in Japan in the 1960s as an antifibrinolytic drug, originally prescribed to reduce bleeding by blocking plasmin from breaking down blood clots. Dermatologists noticed an incidental finding: patients taking oral TXA for surgical or gynecological reasons sometimes saw their melasma fade. That observation launched decades of research into whether the same mechanism could be harnessed for pigmentation management through topical and lower-dose oral administration.
On a skincare label, tranexamic acid appears exactly as "tranexamic acid" or sometimes as its INCI name. It is water-soluble and stable in aqueous formulations, which makes it practical to include in serums and creams. The concentrations used in clinical trials for skin range from 2% to 10% topically, with 2% to 5% being the most studied range for twice-daily at-home application.1
Tranexamic acid was not invented as a skincare ingredient. It was a surgical drug that dermatologists noticed improved pigmentation as a side effect. That origin matters: it has a clearer mechanistic rationale and more clinical data than most actives marketed specifically for dark spots from the outset.
02How tranexamic acid works on skin pigmentation
Most brightening actives target tyrosinase, the enzyme that converts L-DOPA into melanin near the end of the pigmentation pathway. Tranexamic acid does something different: it works earlier in the cascade, interrupting the trigger signal before melanin production ramps up.
The plasminogen connection
When ultraviolet light hits keratinocytes, those cells release plasminogen activators, which convert plasminogen into the protease plasmin. Plasmin, in turn, increases arachidonic acid levels and prostaglandin E2 (PGE2) production. PGE2 is one of the key signals that tells melanocytes to start producing excess melanin. Tranexamic acid works by reversibly blocking lysine-binding sites on plasminogen, preventing plasminogen activators from doing their job.5 Less plasmin means less PGE2, which means less stimulation reaching the melanocytes.
What this means practically
TXA functions as a prevention and suppression tool rather than a direct pigment-removal agent. It reduces the rate of new pigment deposition driven by UV and inflammation. Existing spots do fade as the skin naturally turns over, but TXA is not bleaching existing melanin. This is worth understanding because it sets accurate expectations: you will not see dramatic overnight results, but with consistent use and SPF you are addressing the source of the problem rather than just the surface appearance. It also explains why clinical trials consistently show progressive improvement over 8 to 12 weeks, aligning with the skin's natural renewal cycle.6
For context on how the broader hyperpigmentation pathway connects to other actives like niacinamide, see our guide on niacinamide for hyperpigmentation. And if post-inflammatory marks from past breakouts are part of what you're addressing, the same upstream inflammation mechanism explains why TXA also shows benefit for post-inflammatory hyperpigmentation (PIH), covered further below.
Tranexamic acid works earlier in the pigmentation cascade than most brightening actives. It blocks a UV-triggered signaling chain that would otherwise tell melanocytes to overproduce pigment. That upstream action is its most distinctive feature, and it works best in combination with actives that also target the downstream steps.
03The clinical evidence: what the trials actually show
The evidence base for tranexamic acid and hyperpigmentation is genuinely strong by skincare standards, with multiple randomized controlled trials and several systematic reviews. The picture is more nuanced than most product marketing suggests, so it is worth reading what the studies actually measured.
Topical TXA: the RCT data
A 2012 double-blind split-face RCT applying 5% topical TXA twice daily for 12 weeks found 78% of participants demonstrated reduced melanin on the treated side.1 A separate double-blind trial compared 3% topical TXA against the then-standard combination of 3% hydroquinone plus 0.01% dexamethasone over 12 weeks; both groups showed significant MASI score reductions with no meaningful difference between them, while the TXA group had zero drug-related side effects versus 10% in the hydroquinone group.2 A 2025 randomized clinical trial comparing oral versus topical TXA directly found the topical group (5% cream, twice daily) achieved a 50.88% reduction in melasma severity at 12 weeks, compared to 58.86% for oral.12 Those are comparable outcomes with very different risk profiles.
PIH: post-inflammatory hyperpigmentation
TXA's anti-inflammatory mechanism makes it relevant for PIH, the dark marks left behind after acne, eczema, or skin injury. A 2023 single-blinded RCT compared 5% TXA solution against 20% azelaic acid cream for acne-related PIH over 12 weeks and found comparable improvements at all time points, with TXA showing fewer early side effects.8 A 2022 systematic review of 9 PIH studies across delivery methods confirmed all approaches showed meaningful benefit.9
For more on managing acne-related dark spots, see our guide on how to get rid of acne scars.
What about oral TXA?
Oral tranexamic acid (250 to 500 mg twice daily) shows the strongest results in the literature, including a 2024 meta-analysis of 22 RCTs confirming significant MASI and melanin index reductions.11 However, oral TXA is a prescription medication in most countries, and it carries a meaningfully elevated rate of venous thromboembolism (VTE): a 2021 Danish registry study of 2 million women found an adjusted incidence rate ratio for VTE of approximately 4.7x during TXA exposure periods.10 This is not a reason to avoid topical TXA, but it is a reason not to self-prescribe oral doses based on online recommendations. Topical concentrations are effective, safe, and appropriate for OTC self-care. Oral TXA requires a dermatologist's evaluation and monitoring.
Combination data with niacinamide
A 2014 randomized double-blind trial combined 2% niacinamide with 2% tranexamic acid and found the combination was significantly more effective than vehicle for facial hyperpigmentation at 8 weeks.13 This makes mechanistic sense: niacinamide blocks melanosome transfer from melanocytes to neighboring cells, while TXA reduces upstream signaling. Together they cover two separate intervention points. You can read more about niacinamide's role in our niacinamide guide.
Topical TXA at 2% to 5% has real, replicated clinical evidence behind it. It consistently matches or approaches hydroquinone in trial outcomes while carrying a cleaner tolerability profile. Oral TXA is more potent but carries systemic risks that make it a prescription medication for good reason. For an OTC routine, topical is both effective and safe.
04Alpha arbutin: the downstream complement
If tranexamic acid is the upstream interruption, alpha arbutin is the downstream block. The two actives work at completely different points in the melanogenesis pathway, which is precisely why they pair well.
What alpha arbutin is
Arbutin is a glycosylated form of hydroquinone found naturally in bearberry, cranberry, and several other plants. The alpha form (alpha-arbutin) is the synthetic, more stable, and more potent variant. Unlike hydroquinone, which it structurally resembles, arbutin does not pose the same risk of ochronosis (irreversible skin darkening with long-term use), making it a preferred alternative for sustained use.15
How it works
Alpha arbutin inhibits tyrosinase, the enzyme that catalyzes the rate-limiting step in melanin synthesis: the conversion of L-tyrosine to L-DOPA and of L-DOPA to DOPAquinone. Compared to beta arbutin, alpha arbutin inhibits tyrosinase diphenolase activity significantly more potently, by approximately 10-fold in some enzyme assays, though results vary depending on the enzyme source and substrate used.15 It also inhibits UVB-induced melanin synthesis in cultured cells, adding a photoprotective dimension.
Clinical evidence for alpha arbutin
A 2025 split-face evaluator-blinded pilot study comparing a combination of alpha arbutin 5% plus kojic acid 2% against triple combination cream (hydroquinone, tretinoin, and corticosteroid) for melasma over 12 weeks found no significant difference in melanin index reduction or MASI scores between treatments.16 Importantly, the hydroquinone-based arm showed significantly higher recurrence after discontinuation, and subjects on the arbutin combination had fewer adverse events. A separate 2022 comparative study found arbutin demonstrated significant pigmentation reduction in skin-of-color participants (Fitzpatrick IV-V), outperforming several other single actives including azelaic acid 20% in that cohort.17
For practical layering guidance with vitamin C, which also inhibits tyrosinase through a different mechanism, see our guide on vitamin C serum and skin tone.
Alpha arbutin is a well-tolerated tyrosinase inhibitor with clinical evidence supporting its use across skin tones. It is not as potent as prescription hydroquinone in head-to-head trials, but it avoids hydroquinone's ochronosis risk and carries better tolerability data. Its downstream mechanism makes it a logical complement to TXA's upstream action.
05Brightening actives compared: mechanism, evidence, and practical fit
No single active addresses every point in the pigmentation pathway. The table below maps the most evidence-backed OTC brightening actives by mechanism, evidence level, skin-tone compatibility, and how they fit into a combined routine. No brand names appear; the focus is on the ingredient category and what the research actually supports.
| Active | Where it acts in pathway | Mechanism | OTC concentration range | Evidence level | Skin-tone compatibility | Key consideration |
|---|---|---|---|---|---|---|
| Tranexamic acid | Upstream: signaling | Blocks plasminogen activation; reduces PGE2-driven melanocyte stimulation | 2% - 5% | Strong (multiple RCTs + meta-analyses) | All Fitzpatrick types; validated in III-V | Oral form is prescription-only and carries VTE risk; topical is safe OTC |
| Alpha arbutin | Downstream: enzyme | Reversible tyrosinase inhibitor; blocks melanin synthesis at rate-limiting step | 1% - 5% | Moderate (RCTs; smaller trials) | All types; preferred for skin of color vs hydroquinone | Alpha form is ~10x more potent than beta arbutin in enzyme studies; both are weaker than prescription hydroquinone |
| Niacinamide | Transfer: melanosome | Inhibits transfer of melanosomes from melanocytes to keratinocytes | 2% - 10% | Strong (multiple RCTs including combination data with TXA) | All types; well tolerated | Addresses a different step than TXA or arbutin; highly complementary; also supports barrier function |
| Vitamin C (ascorbic acid) | Downstream: enzyme + antioxidant | Reduces oxidized DOPA back to DOPA; also antioxidant against UV-driven pigmentation triggers | 10% - 20% | Moderate (clinical evidence; formulation-dependent efficacy) | All types; more likely to sting on sensitive or compromised skin at pH below 3.5 | Stability is a real issue; look for L-ascorbic acid at pH 3 to 3.5 in an opaque airtight container |
| Kojic acid | Downstream: enzyme | Chelates the copper ion cofactor tyrosinase needs to function; also antioxidant | 1% - 4% | Moderate (RCTs; often studied in combination) | All types; higher irritation rate than arbutin or TXA; not for compromised skin | Stability concerns in some formulations (kojic acid degrades faster under oxidative stress than its dipalmitate ester) |
| Azelaic acid | Downstream: enzyme + cell turnover | Selective cytostatic effect on abnormally active melanocytes; weak tyrosinase inhibitor | 10% - 20% OTC; 15-20% Rx | Moderate-strong (RCTs; also FDA-cleared for rosacea) | All types; one of the preferred choices in pregnancy | Also has anti-inflammatory and antibacterial properties; addresses PIH from acne particularly well |
| Retinol / retinoids | Multiple: cell turnover + MMP remodeling | Speeds keratinocyte turnover, clearing melanin-rich cells; also some direct tyrosinase inhibition at Rx strengths | 0.025% - 1% OTC retinol | Strong (especially for tretinoin; OTC retinol evidence moderate) | All types but requires sun protection and a careful intro period; higher irritation risk in darker skin tones due to post-inflammatory darkening from purge | Start low and slow; adds photosensitivity; night use only recommended; synergistic with TXA as complementary mechanisms |
The practical takeaway from this table: no single active addresses the entire pigmentation pathway. The strongest approach pairs actives with different mechanisms, which is why TXA plus alpha arbutin plus niacinamide plus daily SPF covers upstream signaling, downstream enzyme inhibition, melanosome transfer, and the UV trigger that starts the whole process. For a deeper look at one of these in isolation, see our niacinamide for hyperpigmentation guide or our breakdown of vitamin C for skin tone.
06How to use tranexamic acid and alpha arbutin together
Both actives are water-soluble, stable at similar pH ranges, and well-tolerated alongside most other skincare ingredients. There are no meaningful compatibility issues between TXA and alpha arbutin, and layering them in a single routine is straightforward.
A simple combined routine
- Morning: Cleanse, apply a vitamin C serum (for antioxidant protection), then a serum containing tranexamic acid and/or alpha arbutin, followed by moisturizer, then SPF 30 or higher. The SPF step is non-negotiable: TXA reduces new pigment formation, but UV exposure continues generating the signals that drive it. Without SPF, you are working against yourself.
- Evening: Cleanse, apply your TXA/arbutin serum, then moisturizer. If you use a retinol or retinoid, apply it on alternating evenings or after your TXA serum to avoid stacking too many exfoliating actives on the same application. Our guide on reducing the look of acne scars covers retinol timing in more detail.
What to avoid combining in the same layer
TXA and alpha arbutin are both broadly compatible actives. The one interaction worth noting: avoid applying an acidic vitamin C (L-ascorbic acid at pH 2.5 to 3.5) in the same layer as your brightening serums if you have sensitive skin, as the low pH can cause stinging over time. A brief wait between layers, or morning vitamin C and evening TXA/arbutin, resolves this without any sacrifice in efficacy.
How long to give it
Allow 8 to 12 weeks before evaluating results. Most clinical trials measure primary outcomes at 8 or 12 weeks, and that aligns with how long it takes for the skin to complete 2 to 3 turnover cycles. Fading of existing spots is gradual. What TXA is doing in the background, reducing the rate of new pigment formation, will not be obviously visible in the first few weeks. Patience and consistent SPF use are what the evidence prescribes.
Daily SPF is not a "nice to have" alongside brightening actives. It is the foundation the entire routine depends on. Every brightening active in the table above works by reducing pigment formation or accelerating pigment clearance. UV exposure restarts pigment formation daily. Without SPF, the math does not work in your favor.
07Skin tone and type considerations
Hyperpigmentation is not equally distributed across Fitzpatrick skin types. People with Fitzpatrick types III to VI have more reactive melanocytes that produce pigment more readily in response to UV and inflammation. This makes the choice of brightening active more consequential: some common ingredients that work fine on lighter skin tones carry real risks for darker skin.
Why tranexamic acid and alpha arbutin are well suited for darker skin tones
Hydroquinone, the historical gold standard for hyperpigmentation treatment, carries a risk of ochronosis (paradoxical darkening) with long-term use, and this risk is higher in darker skin tones. Kojic acid and some aggressive retinoid regimens can also cause post-inflammatory darkening if they provoke irritation on skin that melanogenically "overreacts" to inflammation. Tranexamic acid has no such history. Its mechanism does not involve cytotoxic action on melanocytes, and multiple clinical trials specifically conducted in Fitzpatrick III-V populations confirm both efficacy and excellent tolerability.36 Alpha arbutin also has a clean safety record across skin tones, and arbutin-based formulations outperformed several other single actives in a comparative study specifically using Fitzpatrick IV-V participants.17
Oily and acne-prone skin
Tranexamic acid is water-based and non-comedogenic, so it fits comfortably into routines for oily or acne-prone skin. Post-inflammatory hyperpigmentation (PIH) is often the primary pigmentation concern for this profile, and TXA's anti-inflammatory mechanism addresses the PIH trigger directly. Pairing with niacinamide (which also helps regulate sebum and supports barrier function) makes particular sense for acne-prone skin. For a full discussion of acne-related dark spots, see our guide to reducing acne scars.
Sensitive or reactive skin
Both TXA and alpha arbutin have low irritation profiles and are suitable starting points for sensitive skin. If you are sensitive to the low pH of L-ascorbic acid formulations, consider a more stable vitamin C derivative (ascorbyl glucoside, tetrahexyldecyl ascorbate) or simply separate your vitamin C and brightening steps by time of day. TXA in particular is one of the most recommended brightening actives for sensitive skin precisely because it has no peeling, stinging, or reactive mechanism.
Mature skin
Age spots (solar lentigines) and diffuse UV-related hyperpigmentation are common concerns as skin matures. TXA helps address the UV-triggered signaling driving these, while retinol (used carefully to avoid irritation) accelerates turnover of melanin-rich surface cells. The combination of TXA, alpha arbutin, and a gentle retinol covers the three main levers for this concern. For a broader look at skin aging and actives, our vitamin C serum guide covers the antioxidant dimension in detail.
Browse the full GlowMaxxing collection for MAXXING's skincare lineup.
08Frequently asked questions
Tranexamic acid blocks the interaction between plasminogen and keratinocytes in the skin, which interrupts the UV-triggered cascade that tells melanocytes to produce excess pigment. It also reduces prostaglandin E2, a pro-inflammatory signal that drives melanogenesis. The result is less new pigment being deposited over time, which supports the appearance of more even skin tone. Topical concentrations used in clinical trials range from 2% to 5%, applied twice daily.5
They work through different mechanisms, which is why they complement each other. Tranexamic acid acts upstream by interrupting the keratinocyte-melanocyte signaling that triggers pigment production in the first place. Alpha arbutin acts downstream by directly inhibiting tyrosinase, the enzyme that converts precursors into melanin. Using both addresses two separate points in the pigmentation pathway, which is why combination approaches tend to outperform single actives in clinical research.
Most clinical trials using topical tranexamic acid report meaningful improvement in pigmentation scores at 8 to 12 weeks of twice-daily application. Some participants notice initial changes at 4 weeks. The 2025 RCT comparing oral versus topical TXA found the topical group achieved a 50.88% reduction in MASI scores at 12 weeks.12 Results are gradual and depend heavily on consistent daily SPF use alongside the active.
Yes. Topical tranexamic acid has an excellent safety profile across Fitzpatrick skin types I through VI. Clinical trials specifically conducted in participants with darker skin tones (Fitzpatrick III-V) confirm efficacy and good tolerability.3 Unlike hydroquinone, it does not carry a risk of paradoxical darkening (ochronosis) with prolonged use. It is one of the most recommended ingredients for darker skin tones precisely because of this safety profile.
Yes, and there is clinical evidence supporting the combination. A 2014 randomized double-blind trial found that 2% niacinamide combined with 2% tranexamic acid was significantly more effective than vehicle for reducing facial hyperpigmentation at 8 weeks.13 Both actives are water-soluble and well-tolerated, and they work through complementary mechanisms: niacinamide blocks the transfer of melanosomes from melanocytes to surrounding skin cells, while tranexamic acid reduces the upstream signaling that triggers excess melanin production.
Alpha arbutin is the clinically preferred form. Multiple studies show alpha arbutin inhibits tyrosinase diphenolase activity significantly more potently than beta arbutin at equivalent concentrations.15 Alpha arbutin also has a better safety profile than deoxyarbutin, a related compound that has not received broad regulatory clearance. The European Commission's Scientific Committee on Consumer Safety has approved beta arbutin at up to 7% in face creams with a strict hydroquinone impurity limit, but alpha arbutin is generally the safer and more effective choice for daily topical use.
Not for topical tranexamic acid. Concentrations of 2% to 5% are available in over-the-counter serums and creams without a prescription in most countries. Oral tranexamic acid (250 to 500 mg twice daily) is a prescription medication, and while it shows strong clinical results for melasma, it carries a meaningful elevated risk of venous thromboembolism that requires medical supervision.10 Topical tranexamic acid does not carry systemic VTE risk and is the appropriate choice for OTC self-care.
A solid evidence-based routine combines: daily broad-spectrum SPF 30 or higher (the single most important step), a brightening serum with tranexamic acid and/or alpha arbutin, niacinamide for melanosome transfer inhibition, and optionally a gentle retinol at night for cell turnover. Vitamin C in the morning adds antioxidant protection against UV-driven pigmentation triggers. Consistency and sun protection matter more than any single product choice. Allow 8 to 12 weeks before evaluating results.
Both support the appearance of more even skin tone, but they differ in safety profile. Hydroquinone is the gold-standard prescription active and tends to be more potent in short-term trials, but long-term use carries a risk of ochronosis (paradoxical darkening) and it is prescription-only in many countries. Topical tranexamic acid at 2 to 5% is available OTC, has no ochronosis risk, and is consistently well-tolerated across all Fitzpatrick types. For an OTC routine, tranexamic acid is the more sustainable everyday choice.
They target different steps and often work well together. A 2023 RCT comparing 20% azelaic acid cream versus 5% tranexamic acid for post-inflammatory hyperpigmentation found both actives meaningful, with tranexamic acid showing a slight edge for melanin-driven spots. Azelaic acid also has anti-inflammatory and antibacterial properties, making it particularly useful when pigmentation comes from acne. If your dark spots are from sun or hormonal causes, tranexamic acid tends to be the stronger focused choice.
Tranexamic acid generally has the stronger clinical evidence and a better tolerability profile. Kojic acid inhibits tyrosinase by chelating its copper cofactor, which is effective, but it has a higher irritation rate and stability issues in some formulations. Tranexamic acid works further upstream, has multiple RCTs supporting it across skin tones, and causes far less irritation at typical OTC concentrations. Kojic acid can complement a routine, but tranexamic acid is usually the better anchor active for consistent daily use.
// Sources & references
- Kanechorn Na Ayuthaya P, et al. "Topical 5% tranexamic acid for the treatment of melasma in Asians: a double-blind randomized controlled clinical trial." J Cosmet Laser Ther. 2012;14(3):111-4. PubMed 22506692
- Ebrahimi B, Naeini FF. "Topical tranexamic acid as a promising treatment for melasma." J Res Med Sci. 2014;19(8):753-757. PubMed 25422661
- Lajevardi V, et al. "Comparison of the therapeutic efficacy and safety of combined oral tranexamic acid and topical hydroquinone 4% vs topical hydroquinone 4% alone in melasma." J Cosmet Dermatol. 2017;16(2):235-242. PubMed 27762489
- Wu S, et al. "Randomised, controlled, double-blind study of combination therapy of oral tranexamic acid and topical hydroquinone in the treatment of melasma." Australas J Dermatol. 2020;61(2):e167-e173. PubMed 32109318
- Sheth VM, Pandya AG. "Melasma: a comprehensive update: part II." J Am Acad Dermatol. 2011. Review covering TXA mechanism via plasminogen inhibition and arachidonic acid pathway. PubMed 21821313. Also: Holloway VL. "Tranexamic acid in treatment of melasma: a comprehensive review." Dermatol Ther. 2017. PubMed 28133910
- Taraz M, et al. "Tranexamic acid in melasma: a focused review on drug administration routes." J Cosmet Dermatol. 2023;22(1):44-51. PubMed 36606378
- Kim EH, et al. "Clinical efficacy of topical tranexamic acid with microneedling in melasma." Dermatol Surg. 2020;46(10):1336-1342. PubMed 32769524
- Rafiei R, et al. "Comparative study of 20% azelaic acid cream versus 5% tranexamic acid solution for the treatment of postinflammatory hyperpigmentation in acne vulgaris." J Res Med Sci. 2023;28:37. PubMed 37213446
- Davis EC, Callender VD. "Efficacy and best mode of delivery for tranexamic acid in post-inflammatory hyperpigmentation: a systematic review." Clin Cosmet Investig Dermatol. 2022;15:2803-2815. PubMed 36597522
- Sundstrom A, et al. "Oral tranexamic acid and thrombosis risk in women." EClinicalMedicine. 2021;38:100882. PubMed 34124632
- Colferai MM, et al. "Efficacy and safety of tranexamic acid in the treatment of adult melasma: An updated meta-analysis." J Clin Pharm Ther. 2021;46(5):1284-1297. PubMed 33959984
- Saleh FY, et al. "Randomized clinical trial on the efficacy of oral tranexamic acid versus topical tranexamic acid in treatment of melasma." J Cosmet Dermatol. 2025. PMC12418907
- Hakozaki T, et al. "Reduction in facial hyperpigmentation after treatment with a combination of topical niacinamide and tranexamic acid: a randomized, double-blind, vehicle-controlled trial." Skin Res Technol. 2014;20(2):206-210. PubMed 24033822
- Holloway VL. "Tranexamic Acid for Hyperpigmentation Disorders: A Literature Review on Efficacy and Safety in Melasma and PIH." J Cosmet Dermatol. 2026. PMC12848551
- Rzepka Z, et al. "Arbutin as a skin depigmenting agent with antimelanogenic and antioxidant properties." Antioxidants (Basel). 2021;10(7):1129. PubMed 34356362
- Panyatip P, et al. "The efficacy of topical cosmetic containing alpha-arbutin 5% and kojic acid 2% compared with triple combination cream for the treatment of melasma: a split-face, evaluator-blinded randomized pilot study." J Cosmet Dermatol. 2025. PubMed 39555866
- Abas ZA, et al. "Comparative study on depigmenting agents in skin of color." J Clin Aesthet Dermatol. 2022;15(2):23-30. PMC8884189
