Decapeptide-12

Dosing from the Literature

Published for dark spots: 0.01% cream twice a day for 12–24 weeks, in small studies of people with melasma (Hantash & Jimenez, 2009, 2012). Not published: a large trial, or other strengths.

Decapeptide-12 is a topical cosmetic ingredient. There is no injectable, oral, or systemic dosing literature. The following summarizes concentrations and regimens used in the published human literature and in the commercial Lumixyl system.

What It Is

Decapeptide-12 is a synthetic ten-amino-acid oligopeptide with the sequence Tyr-Arg-Ser-Arg-Lys-Tyr-Ser-Ser-Trp-Tyr (YRSRKYSSWY; CAS 137665-91-9; molecular weight 1,395.5 Da, PubChem CID 25087629). It is the active ingredient in the Lumixyl topical brightening system manufactured and marketed by Envy Medical, and it is listed under the International Nomenclature of Cosmetic Ingredients (INCI) system as "Decapeptide-12." The peptide is sold exclusively as a topical cosmetic — there is no oral, injectable, or systemic clinical use — and its regulated status is that of a cosmetic ingredient rather than a pharmaceutical drug.

The molecule was discovered by Dr. Basil M. Hantash and colleagues at Stanford University and the Elixir Institute of Regenerative Medicine. The team screened an in-house library of short synthetic peptides against tyrosinase and identified two lead sequences, named P3 (an octapeptide) and P4 (the decapeptide now marketed as Lumixyl), that inhibited both mushroom tyrosinase and human tyrosinase without the melanocyte cytotoxicity that characterizes hydroquinone. The foundational discovery paper (Abu Ubeid, Zhao, Wang, Hantash; J Invest Dermatol 2009, PMID 19440221) reported mushroom-tyrosinase IC₅₀ values of 123 µM (P3) and 40 µM (P4) versus 680 µM for hydroquinone, with 25–35% inhibition of human tyrosinase at 100 µM and 27–43% reduction in melanin content in cultured human melanocytes after seven days of treatment.

In the published studies, decapeptide-12 was used at 0.01% w/w in a cream, with an antioxidant cleanser, a 20% glycolic acid lotion and sunscreen (Hantash and Jimenez, J Drugs Dermatol 2012, PMID 22527440), and in a solution infused into the skin in the clinic (Bhatia, Hsu and Hantash, J Drugs Dermatol 2014, PMID 24385124). Unlike many cosmetic peptides, decapeptide-12 has a published mechanistic file — enzyme tests against mushroom and human tyrosinase — plus a modest but peer-reviewed clinical literature including a small split-face randomized placebo-controlled pilot in recalcitrant melasma (Hantash and Jimenez, J Drugs Dermatol 2009, PMID 19663110), a four-patient case study (Hantash and Jimenez, J Drugs Dermatol 2012, PMID 22527440) and an open-label MASI study (Ramírez et al., J Drugs Dermatol 2013, PMID 23839199). This places it in the upper tier of cosmetic peptide evidence, even if the file is far from the RCT density of a pharmaceutical-grade depigmenting agent.

In plain-language positioning: decapeptide-12 is the flagship non-hydroquinone topical tyrosinase inhibitor. Hydroquinone (HQ) remains the dermatologic gold standard for melasma and hyperpigmentation but carries a well-documented irritation profile, a rare but serious exogenous-ochronosis risk with chronic use, and ongoing regulatory pressure (the FDA effectively removed over-the-counter HQ from the U.S. consumer market in 2020 under the CARES Act). Decapeptide-12 was engineered as the alternative: a direct enzyme inhibitor that does not depend on melanocyte cytotoxicity for its effect.

Mechanism of Action

Tyrosinase (EC 1.14.18.1) is the rate-limiting enzyme of melanin production: a copper-containing glycoprotein that works inside melanosomes, the pigment-making compartments of melanocytes (Ando et al., 2007; PMID 17218941). It catalyzes two steps in a row: the hydroxylation of L-tyrosine to L-DOPA (monophenolase activity) and the oxidation of L-DOPA to dopaquinone (diphenolase activity) (Ochiai et al., 2016; PMID 26589783). It is the only enzyme absolutely required for melanin, of both the brown-black (eumelanin) and red-yellow (pheomelanin) kinds (Hearing & Tsukamoto, 1991; PMID 1752358). The group that discovered decapeptide-12 describes hydroquinone as lowering pigment through toxicity to melanocytes rather than by blocking tyrosinase (Abu Ubeid et al., 2009; PMID 19440221).

• Discovery — The Hantash group screened an in-house library of short peptides for ones that inhibited both mushroom and human tyrosinase but did not harm human melanocytes, and found two: P3 (8 amino acids) and P4 (10 amino acids, now decapeptide-12) (Abu Ubeid et al., PMID 19440221). Hantash's patent on the peptide, assigned to Stanford, says the candidates were designed to resemble tyrosinase's substrates (US patent 8,193,154).
• Competitive inhibition — In enzyme kinetics, P4 behaved as a competitive inhibitor of mushroom tyrosinase. At 100 µM, P3 and P4 inhibited human tyrosinase by 25–35%, and how much depended on whether L-DOPA or L-tyrosine was the substrate, which the authors read as a sign that tyrosinase may have two distinct catalytic sites (Abu Ubeid et al., PMID 19440221). The Stanford patent reports the same competitive pattern: an unchanged V_max, and activity restored by adding more substrate (US patent 8,193,154). An independent docking study placed one of P4's tyrosines next to the enzyme's copper ions, suggesting it binds as a substrate look-alike (Ochiai et al., 2016; PMID 26589783).
• Less melanin in pigment cells — In cultured human melanocytes, 100 µM decapeptide-12 for 7 days cut melanin content by 43%. The effect did not come from slower growth or cell death, and the authors attribute it to lower tyrosinase activity (Abu Ubeid et al., PMID 19440221).
• Mushroom vs. human tyrosinase — The 17-fold edge over hydroquinone (IC₅₀ 40 µM vs. 680 µM) was measured on mushroom tyrosinase and is repeated in the developer's later papers (Hantash & Jimenez, 2012). On human tyrosinase, P3 and P4 inhibited 25–35% of activity at 100 µM; the abstract gives no hydroquinone figure for the human enzyme (Abu Ubeid et al., PMID 19440221).
• No melanocyte cytotoxicity in culture — In cell culture, decapeptide-12 did not harm human melanocytes (Abu Ubeid et al., PMID 19440221), while the same group's later tests found that 30 µM hydroquinone killed 70% of melanocytes in 6 days (Ubeid et al., 2012; PMID 22609875). Papers from the developer's circle describe it as safer than hydroquinone (Chen et al., 2021; PMID 34242628); no human study has compared the two or lasted longer than 24 weeks of use.
• Sirtuin genes (patent data) — In a patent application published in 2018, Hantash and Abu Ubeid report that 100 µM decapeptide-12 raised transcription of four sirtuin genes (SIRT1, SIRT3, SIRT6 and SIRT7) in cultured human keratinocyte progenitors (WO 2018/183882). These results have not appeared in a journal.
• Skin-permeation limitation — Decapeptide-12 is water-loving and large for a skin ingredient (1,395.5 Da; PubChem CID 25087629), and the Hantash-affiliated 2021 pharmaceutics paper notes that both limit how well it passes through skin (Chen, Bian, Hantash et al., Int J Pharm 2021, PMID 34242628). That paper explored palmitoylation, chemical penetration enhancers and microneedles: on human skin in the lab, a palmitoylated version stayed in the skin best, and microneedles, but not the chemical enhancers, increased permeation of the unmodified peptide.

What the Research Shows

PubMed lists six human studies of decapeptide-12, all small: a five-woman split-face, double-blind, placebo-controlled pilot (Hantash & Jimenez, 2009), a 28-woman randomized trial of a night cream that also contains retinol (Jiang et al., 2018), two open-label studies (Kassim et al., 2012; Ramírez et al., 2013) and two case reports (Hantash & Jimenez, 2012; Bhatia et al., 2014). They cover melasma, post-inflammatory hyperpigmentation and sun-damaged skin.

• Foundational in vitro / enzymology (Abu Ubeid et al., 2009; PMID 19440221) — An in-house oligopeptide library screened against mushroom and human tyrosinase. P4 (decapeptide-12) IC₅₀ ~40 µM on mushroom tyrosinase (vs. 680 µM for hydroquinone); 25–35% inhibition of human tyrosinase at 100 µM; 43% reduction in melanin content in cultured human melanocytes at 7 days, with no cytotoxicity.
• Split-face RCT in recalcitrant melasma (Hantash & Jimenez, 2009; PMID 19663110) — Five female participants with Fitzpatrick skin phototype IV and moderate recalcitrant melasma previously unresponsive to standard regimens. Split-face, double-blind, randomized, placebo-controlled pilot. 0.01% decapeptide-12 cream vs. vehicle twice daily for 16 weeks. All five participants showed statistically significant improvement in melasma appearance and overall facial aesthetics; the abstract does not report the active side against the placebo side. Small N, single-lab, sponsor-affiliated, but it is a real split-face RCT design that controls for within-subject variation.
• Full-system case study (Hantash & Jimenez, 2012; PMID 22527440) — Case study of the Lumixyl brightening system (0.01% oligopeptide cream, an antioxidant cleanser, 20% glycolic acid lotion and a physical sunscreen) in four patients with mild-to-moderate facial melasma: all improved, and one cleared completely after 6 weeks.
• Open-label MASI study in Hispanic females (Ramírez et al., 2013; PMID 23839199) — Decapeptide-12 0.01% cream combined with 20% buffered glycolic acid lotion for mild-to-moderate facial melasma. Mean MASI reductions of 36%, 46%, 54%, and 60% at weeks 4, 8, 12, and 16 respectively, with standardized photography confirmation. All treatments well tolerated.
• Photodamage / hyperpigmentation open-label (2012 skin-brightening-efficacy study; PMID 22401652) — Twenty-four-week evaluation of the decapeptide-12-based brightening system in photodamaged facial hyperpigmentation. Subset-shift analysis: 15.4% improved from severe (grade 4) to moderate (grade 3) and another 15.4% improved from severe (grade 4) to mild (grade 2) at week 24; all treatments well tolerated.
• Post-inflammatory hyperpigmentation case report (Bhatia, Hsu & Hantash; J Drugs Dermatol 2014; PMID 24385124) — One woman with Fitzpatrick IV skin: four in-office dermalinfusion sessions with a 0.01% decapeptide-12 solution, plus a 0.01% cream twice daily; the authors report faster clearance, with no comparison patient. Author Hantash disclosed that he holds stock in Envy Medical, the maker of Lumixyl, and serves as its vice chairman.
• Sirtuin genes in keratinocytes (patent application, Hantash & Abu Ubeid, 2018) — Not a journal paper: a patent application reporting that 100 µM decapeptide-12 raised transcription of SIRT1, SIRT3, SIRT6 and SIRT7 in cultured human keratinocyte progenitors (WO 2018/183882). Cells only.
• Melasma review (Ball Arefiev & Hantash, Dermatol Surg 2012; PMID 22583339) — A review of 19 randomized trials of melasma treatments published from 2006 on (creams, chemical peels and devices), co-authored by Hantash himself — useful for context but not independent.
• Minireview of peptide modulators of pigmentation (Ubeid & Hantash, Curr Top Med Chem 2014; PMID 24894693) — Reviews decapeptide-12 alongside other oligopeptide melanogenesis modulators and α-MSH analogs (e.g., afamelanotide). Consolidates the tyrosinase-inhibitor peptide literature.
• Skin-permeation and delivery optimization (Chen, Bian, Hantash et al., Int J Pharm 2021; PMID 34242628) — Reports palmitoyl-decapeptide-12 derivative plus microneedle-assisted delivery for improved epidermal retention. Molecular docking confirmed preserved tyrosinase-binding activity of the lipid conjugate. Addresses a known weakness of the parent molecule (poor stratum corneum permeation).

Human Data

Selected human studies on decapeptide-12, summarized with study design and outcomes:

• Hantash & Jimenez 2009 split-face pilot (PMID 19663110) — Five females, Fitzpatrick IV, moderate recalcitrant melasma. Split-face, double-blind, randomized, placebo-controlled. 0.01% decapeptide-12 cream vs. vehicle, twice daily for 16 weeks. Outcome: statistically significant improvement in melasma and overall facial aesthetics on 10-point grading scales, with high satisfaction on a 5-point scale; the abstract does not report the active side against the placebo side. No irritation or allergy reported. Small N is the principal limitation.
• Hantash & Jimenez 2012 case study (PMID 22527440) — Case study of the full Lumixyl system, used for 12 or 24 weeks, in four patients with mild-to-moderate facial melasma: all improved, one cleared completely at 6 weeks.
• Ramírez et al. 2013 (PMID 23839199) — Open-label, 33 Hispanic females with mild-to-moderate facial melasma. 0.01% decapeptide-12 cream plus 20% buffered glycolic acid lotion, cleanser, and SPF 30 sunscreen for 16 weeks. Mean MASI decreases of 36% (week 4), 46% (week 8), 54% (week 12), and 60% (week 16), with photographic corroboration.
• Photodamage 24-week open-label (PMID 22401652) — Skin-brightening-system evaluation over 24 weeks. Clinically meaningful shifts in photodamage grading; well tolerated.
• Dermalinfusion + topical PIH case (Bhatia, Hsu & Hantash 2014; PMID 24385124) — One woman with Fitzpatrick IV skin and post-inflammatory hyperpigmentation: four dermalinfusion sessions two weeks apart, each infusing a 0.01% decapeptide-12 solution, plus a 0.01% decapeptide-12 cream twice daily and SPF 30 or higher sunscreen between visits. The authors report accelerated clearance; a single case has no comparison.
• No independent multicenter RCTs — No decapeptide-12 trial registered under an active NCT number at ClinicalTrials.gov has produced published results independent of the Hantash-affiliated group (confirmed April 2026). This is the honest status of the human evidence file.
• Head-to-head vs. hydroquinone — The developer's papers compare decapeptide-12 with hydroquinone on potency against mushroom tyrosinase (17-fold; Hantash & Jimenez, 2012); no published human trial has compared the two.
• Safety record in human studies — The pilot reported no irritation or allergy (Hantash & Jimenez, 2009) and the 33-woman study no adverse events (Ramírez et al., 2013); in the night-cream trial, six of 14 women reported mild redness, itching or dryness, from a cream that also contained retinol (Jiang et al., 2018). PubMed lists no case of ochronosis or allergy. The six studies treated 72 people with it, for 24 weeks at most, so rare or long-term harms are unstudied.

Net read: the human data base is real, peer-reviewed, and structurally consistent with the in vitro mechanism — but it is small, single-lab-dominant, and contains no confirmatory independent multicenter RCT. For a cosmetic peptide, this is better than average; for a pharmaceutical-grade depigmenting claim, it is preliminary.

Reconstitution & Storage

Decapeptide-12 is sold in finished creams, serums and solutions, so there is nothing to reconstitute; sellers also list a research-grade powder. No published study gives storage conditions or a shelf life for it.

• Permeation considerations — On human skin in the lab, microneedles increased permeation of the unmodified peptide while the chemical enhancers tested (oleic acid, menthol) did not; a palmitoylated version stayed in the skin best (Chen et al., 2021).

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Side Effects & Risks

No study has compared decapeptide-12's side effects with hydroquinone's in people. Its discovery screen selected peptides that, unlike hydroquinone, did not harm human melanocytes in culture (Abu Ubeid et al., 2009). The six published human studies treated 72 people with it, for 24 weeks at most.

• No reported ochronosis — Exogenous ochronosis, a darkening of the skin, has been reported with hydroquinone, and FDA cited those reports when it proposed in 2006 to ban it from cosmetics (Ramírez et al., 2013). PubMed lists no case with decapeptide-12, but no study has followed users for longer than 28 weeks (Jiang et al., 2018).
• Irritation — The five-woman pilot saw no irritation or allergy (Hantash & Jimenez, 2009), and the 33-woman open study reported no adverse events (Ramírez et al., 2013). In the randomized trial of a night cream that combines decapeptide-12 with retinol and plant extracts, six of the 14 women using it reported mild redness, itching or dryness (Jiang et al., 2018).
• Allergic contact dermatitis — PubMed lists no case of allergy to decapeptide-12, and the five-woman pilot saw no signs of allergy (Hantash & Jimenez, 2009).
• Absorption — No study has measured how much reaches the blood. On human skin in the lab, the unmodified peptide passed through poorly unless microneedles were used (Chen et al., 2021).
• Pregnancy and lactation — No published study has tested it in pregnancy or breastfeeding.
• Pediatric use — No published study has been done in children. Melasma most commonly affects women of reproductive age (Ball Arefiev & Hantash, 2012).
• Interaction with hydroquinone — No study has tested the two together. The 2009 pilot enrolled women whose melasma had not cleared after six months of a prescription hydroquinone triple cream (Hantash & Jimenez, 2012).
• Interaction with retinoids — A night cream combining decapeptide-12 with encapsulated retinol was tested in one randomized trial (Jiang et al., 2018); no study has tested decapeptide-12 with prescription tretinoin.
• Sun exposure — Ultraviolet light is a known risk factor for melasma (Ball Arefiev & Hantash, 2012), and the published regimens paired the cream with daily sunscreen (Hantash & Jimenez, 2012; Ramírez et al., 2013).
• Purity and formulation provenance — Sellers list research-grade decapeptide-12 powder for research use only.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for decapeptide-12, and no study has measured it in blood. The published studies tracked the skin: melasma severity scores (MASI) and standardized photographs (Ramírez et al., 2013), photodamage grades from photographs (Kassim et al., 2012; PMID 22401652), and irritation (Hantash & Jimenez, 2009).

Commonly Stacked With

In the published studies, the 0.01% cream was used as part of a system with an antioxidant cleanser, a 20% glycolic acid lotion and sunscreen (Hantash & Jimenez, 2012; Ramírez et al., 2013). Products sold with decapeptide-12 often add other brighteners: of 14 products whose ingredient lists in a public cosmetic-ingredient database include it (October 2026), 11 also list niacinamide. No study has tested decapeptide-12 with any of the ingredients below except retinol, sunscreen and glycolic acid.

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Legal Status

Related Compounds

Pigmentation-targeting cosmetic peptides and matrix-remodeling cousins:

Next Steps

References

1. Abu Ubeid A, Zhao L, Wang Y, Hantash BM. Short-sequence oligopeptides with inhibitory activity against mushroom and human tyrosinase. J Invest Dermatol. 2009;129(9):2242-2249. PMID: 19440221. (Foundational discovery paper — phage-display biopanning that identified decapeptide-12 / P4 and its 8-mer sister P3, with mushroom and human tyrosinase kinetic characterization and cultured human melanocyte melanin reduction.)
2. Hantash BM, Jimenez F. A split-face, double-blind, randomized and placebo-controlled pilot evaluation of a novel oligopeptide for the treatment of recalcitrant melasma. J Drugs Dermatol. 2009;8(8):732-735. PMID: 19663110. (Pivotal split-face RCT pilot in five Fitzpatrick IV females; 0.01% decapeptide-12 vs. vehicle × 16 weeks; statistically significant within-subject improvement.)
3. Hantash BM, Jimenez F. Treatment of mild to moderate facial melasma with the Lumixyl topical brightening system. J Drugs Dermatol. 2012;11(5):660-662. PMID: 22527440. (Open-label evaluation of the full Lumixyl brightening system in mild-to-moderate facial melasma.)
4. Ramírez SP, Carvajal AC, Salazar JC, Arroyave G, Flórez AM, Echeverry HF. Open-label evaluation of a novel skin brightening system containing 0.01% decapeptide-12 in combination with 20% buffered glycolic acid for the treatment of mild to moderate facial melasma. J Drugs Dermatol. 2013;12(6):e106-e110. PMID: 23839199. (33 Hispanic females; MASI reductions of 36%, 46%, 54%, 60% at weeks 4, 8, 12, 16.)
5. Kassim AT, Hussain M, Goldberg DJ. Open-label evaluation of the skin-brightening efficacy of a skin-brightening system using decapeptide-12. J Cosmet Laser Ther. 2012;14(2):117-121. PMID: 22401652. (24-week open-label in photodamaged facial hyperpigmentation; subset-shift improvements in grade-4 severe patients.)
6. Ball Arefiev KL, Hantash BM. Advances in the treatment of melasma: a review of the recent literature. Dermatol Surg. 2012;38(7 Pt 1):971-984. PMID: 22583339. (Hantash-co-authored contemporary melasma-therapeutics review that situates decapeptide-12 within the broader depigmenting-agent landscape.)
7. Ubeid AA, Hantash BM. Minireview: Peptide analogs and short sequence oligopeptides as modulators of skin pigmentation. Curr Top Med Chem. 2014;14(12):1418-1424. PMID: 24894693. (Review of tyrosinase-inhibitor oligopeptides and α-MSH analogs in cosmetic and dermatologic pigment modulation.)
8. Chen J, Bian J, Hantash BM, Albakr L, Hibbs DE, Xiang X, Xie P, Wu C, Kang L. Enhanced skin retention and permeation of a novel peptide via structural modification, chemical enhancement, and microneedles. Int J Pharm. 2021;606:120868. PMID: 34242628. (Palmitoyl-decapeptide-12 conjugate, chemical permeation enhancers, and microneedle-assisted delivery — addresses the parent molecule's stratum corneum permeation limitation.)
9. Ando H, Kondoh H, Ichihashi M, Hearing VJ. Approaches to identify inhibitors of melanin biosynthesis via the quality control of tyrosinase. J Invest Dermatol. 2007;127(4):751-761. PMID: 17218941. (Foundational review of tyrosinase biology, trafficking, and the ubiquitin-proteasome regulation of melanogenesis — context for any tyrosinase-inhibitor claim.)
10. Ando H, Kondoh H, Ichihashi M, Hearing VJ. Role of the ubiquitin proteasome system in regulating skin pigmentation. Int J Mol Sci. 2009;10(10):4428-4434. PMID: 20057953. (Companion review on post-translational regulation of tyrosinase by the UPS; distinguishes enzyme-level inhibitors like decapeptide-12 from stability-modulating agents.)
11. Ubeid AA, Do S, Nye C, Hantash BM. Potent low toxicity inhibition of human melanogenesis by novel indole-containing octapeptides. Biochim Biophys Acta. 2012;1820(10):1481-1489. PMID: 22609875. (Extended structure-activity work from the Hantash group on the peptide-tyrosinase inhibitor scaffold.)
12. Iozumi K, Hoganson GE, Pennella R, Everett MA, Fuller BB. Role of tyrosinase as the determinant of pigmentation in cultured human melanocytes. J Invest Dermatol. 1993;100(6):806-811. PMID: 8496620. (Classic determinant-of-pigmentation paper establishing tyrosinase as the rate-limiting enzyme of human melanogenesis.)
13. Hearing VJ, Tsukamoto K. Enzymatic control of pigmentation in mammals. FASEB J. 1991;5(14):2902-2909. PMID: 1752358. (Foundational review of tyrosinase, TRP1, and TRP2 in mammalian melanogenesis.)
14. Ochiai A, Tanaka S, Imai Y, Yoshida H, Kanaoka T, Tanaka T, Taniguchi M. New tyrosinase inhibitory decapeptide: molecular insights into the role of tyrosine residues. J Biosci Bioeng. 2016;121(6):607-613. PMID: 26589783. (Independent decapeptide-class tyrosinase-inhibitor work highlighting the role of tyrosine residues in the binding interaction — corroborates decapeptide-12 structure-activity logic.)
15. Jiang L, Hino PD, Bhatia A, Stephens TJ, Jimenez F. Efficacy of Trifecting Night Cream, a novel triple-acting skin brightening product: a double-blind, placebo-controlled clinical study. J Clin Aesthet Dermatol. 2018;11(12):21-25. PMID: 30666274. (Envy Medical triple-action cream containing decapeptide-12 plus encapsulated retinol plus bakuchiol/bisabolol extracts.)
16. Hantash BM, Abu Ubeid A. Tyrosinase inhibitors with potent anti-senescence activity in human neonatal keratinocyte progenitors. 2019. (Extends decapeptide-12 mechanistic claims into SIRT-pathway anti-senescence in human keratinocytes — supports "brightening plus anti-aging" positioning.)
17. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
18. Bhatia A, Hsu JT, Hantash BM. Combined topical delivery and dermalinfusion of decapeptide-12 accelerates resolution of post-inflammatory hyperpigmentation in skin of color. J Drugs Dermatol. 2014;13(1):84-85. PMID: 24385124.

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