Compound Guides

What GLOW Peptide Does to Your Bloodwork (And Copper Levels)

Bruno SouzaBruno Souza29 May 202621 min readSupport My TRT
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What GLOW Peptide Does to Your Bloodwork (And Copper Levels)

Most articles about GLOW peptide repeat the same vendor copy: skin glow, faster recovery, gut healing, run it 8 to 12 weeks. None of them mention that you're injecting 316mcg of elemental copper every time you draw a 2mg GHK-Cu dose. Over an 8-week daily cycle, that's 17.7mg of copper bypassing your gut and going straight into your bloodstream. The Tolerable Upper Intake Level for oral copper is 10mg/day. This is a math problem nobody is doing.

This is harm-reduction commentary, not medical advice. BPC-157, TB-500, and GHK-Cu are not approved by any regulator for systemic injection in humans. All three lack published human dose-response trials. Talk to a clinician before injecting peptides, especially if you're already on TRT, AAS, or any hepatotoxic compound.

Quick answer: A standard GLOW vial contains 50mg GHK-Cu, 10mg BPC-157, and 10mg TB-500 in a fixed 5:1:1 ratio. Each 2mg GHK-Cu dose also delivers 400mcg BPC-157, 400mcg TB-500, and about 316mcg of elemental copper. Run a baseline panel before starting: ALT, AST, GGT, hs-CRP, ferritin, albumin, serum copper, ceruloplasmin. Recheck at week 4 and week 12. The two markers nobody talks about are serum copper above 155mcg/dL and calculated free copper above 25mcg/dL. Full evidence review and protocol below.

What's actually in a GLOW vial

GLOW is a vendor-formulated blend. There is no FDA-approved version, no clinical trial, and no published evidence that the specific 5:1:1 ratio is optimal for anything. What there is, surprisingly, is consistency across vendors. Almost every reputable peptide vendor selling GLOW uses the same composition:

Total: 70mg per vial, ratio 5:1:1. PeptideFox, Verified Peptides, Cosmic Peptides, Alpha Omega, and most US compounding pharmacies converge on this formulation. The "LL-37 + Oxytocin + Wormwood" version that shows up on a few fringe vendor pages is almost certainly a confusion with the unrelated "Wolverine Stack." Ignore it.

The TB-500 labeling problem

There is one ambiguity in every GLOW vial that you cannot resolve without a mass spec: what's actually labeled "TB-500" might not be TB-500. Real TB-500, per the doping-control literature, is the synthetic acetylated heptapeptide Ac-LKKTETQ (the 17-23 fragment of full-length thymosin beta-4). Esposito et al., 2012 showed analytically that vials labeled "TB-500" sometimes contain full-length 43-amino-acid TB-4 instead. Labels are used interchangeably across vendors. The full-length protein is the one with most of the published clinical data (Ruff et al., 2010; Sosne et al., 2015). The 7-amino-acid fragment is what most vendors actually claim to sell. You usually have no way to verify which you received.

For this article, "TB-500" means "whatever your vendor put in the vial," and the dosing math assumes the fragment by default.

The 2mg anchor math

The standard GLOW protocol anchors on 2mg of GHK-Cu per injection, drawn as 0.1mL from a 70mg vial reconstituted in 2.5mL of bacteriostatic water. Because the ratio is fixed at 5:1:1, the same 0.1mL draw delivers:

  • GHK-Cu: 2mg (2,000mcg)
  • BPC-157: 400mcg
  • TB-500: 400mcg

The copper math is the part that gets skipped. GHK-Cu is glycyl-L-histidyl-L-lysine coordinated to a Cu(II) ion. Molecular weight is approximately 401.9 g/mol. Copper's atomic weight is 63.55 g/mol. So the elemental copper fraction is 63.55 / 401.9 = 15.8% by mass.

Plugged into the GLOW dose:

  • 50mg GHK-Cu per vial = ~7.9mg elemental copper per vial
  • 2mg GHK-Cu per injection = ~316mcg elemental copper per dose
  • Daily for 8 weeks = ~17.7mg cumulative elemental copper, subcutaneous

For comparison, the adult Recommended Daily Allowance for copper is 900mcg/day, and the Tolerable Upper Intake Level (UL) is 10mg/day. The UL is set on oral intake, where intestinal absorption is tightly regulated. Subcutaneous injection bypasses that regulation entirely. Every microgram of copper from a GLOW dose is bioavailable.

This is not a Wilson's disease scenario. Wilson's is copper underclearance. GLOW is potential copper overload via a route nobody has studied at chronic timepoints in humans. The right frame is iatrogenic copper loading, not genetic disease, but the lab markers used to monitor Wilson's are the closest available tools.

Bodyweight-titrated dosing (the gap nobody covers)

Every published GLOW protocol uses the same fixed 2mg GHK-Cu draw regardless of who you are. A 50kg female athlete and a 110kg male bodybuilder draw the same volume. This makes no pharmacological sense if you think about the BPC-157 dose:

  • 50kg user: 400mcg BPC-157 = 8mcg/kg
  • 70kg user: 400mcg BPC-157 = 5.7mcg/kg
  • 110kg user: 400mcg BPC-157 = 3.6mcg/kg

The Sikiric group, which has published most of the BPC-157 preclinical literature, commonly uses doses in the 10mcg/kg range in rats across their gastroprotection, tendon, and ligament work (Sikiric et al., 2014; Chang et al., 2014). At the standard GLOW draw, a 50kg user is hitting the rat reference. A 110kg user is at 36% of it. The same fixed volume is supratherapeutic for the small woman and subtherapeutic for the large man.

Per-kg titration works against the user, too. Animal-to-human dose conversion typically uses the FDA allometric scaling formula, which divides the rodent dose by about 6.2. Applied to Sikiric's 10mcg/kg rat dose, the human-equivalent dose is closer to 1.6mcg/kg. At that number, the standard 400mcg BPC-157 draw is well above the rat-equivalent for everyone, regardless of weight. The honest answer is that nobody knows the right human dose for BPC-157, and the per-kg argument is directionally useful but not authoritative.

What you can do:

BodyweightGLOW drawBPC-157 (mcg/kg)GHK-Cu (mg)Copper (mcg)
50kg0.05-0.07mL4-5.6mcg/kg1-1.4158-221
70-85kg0.1mL (default)4.7-5.7mcg/kg2.0316
90-110kg0.12-0.15mL4.9-6.3mcg/kg2.4-3.0379-474

These are extrapolations, not validated doses. The case for titrating down on a smaller user is the copper load: a 50kg woman injecting the default 0.1mL gets 6.3mcg of copper per kg of body weight per day, vs 2.9mcg/kg for an 110kg male. That's a 2.2x difference in chronic copper exposure relative to body mass.

The bloodwork panel, mapped to GLOW components

Each component of GLOW maps to a different set of markers. The panel below is the one I'd run at baseline, week 4, and week 12, with trigger thresholds for each.

Baseline (before any injection)

You want to know where you started before any GLOW dose hits your system. The full panel:

  • ALT, AST, GGT, total bilirubin: liver function. BPC-157 is hepatoprotective in rats (Sikiric et al., 1993). Whether that translates to humans is unknown, and if you're on AAS, the steroid noise will swamp any peptide signal.
  • hs-CRP: systemic inflammation. The mechanistic case for BPC-157 lowering inflammation is strong in preclinical models. The human case is non-existent. No published RCT has measured CRP response to BPC-157 in humans. The only safety pilot (Lee & Burgess, 2025) was 2 people at 20mg IV with no biomarker change.
  • Ferritin, iron: iron status, plus inflammation marker (ferritin is an acute-phase reactant). If GLOW lowers inflammation, ferritin trends down. If it drives tissue remodeling that consumes iron, ferritin also trends down. Direction is theoretical, not predictable.
  • Albumin: protein status. GHK-Cu drives collagen synthesis, which needs amino acid substrate. Low albumin means you don't have the raw material for the response GLOW is supposed to deliver.
  • Serum copper: 70-140mcg/dL reference range. This is the core GLOW marker.
  • Ceruloplasmin: 20-35 mg/dL reference range. Liver-produced, binds about 90% of serum copper in health.
  • Calculated free copper: total Cu minus (ceruloplasmin × 3). Normal range 5-15mcg/dL. The Walshe formula is the standard.

If you can afford it, add a 24-hour urinary copper at baseline (under 30mcg/day normal). It's the most reliable accumulation marker we have.

Week 4 (early tolerability check)

The repeat panel is the same as baseline. Triggers at week 4:

MarkerFlagAction
ALT or AST>2x ULNCheck GGT; see decision tree below
GGT>2x ULNHepatic origin confirmed; investigate
hs-CRP>3 mg/LInvestigate infection, AAS hepatic stress, not BPC-157
Ferritindrop >50%Iron panel; rule out inflammation masking
Serum copper>140mcg/dLHold GHK-Cu, recheck in 4 weeks
Ceruloplasminunder 20 mg/dL with high CuWilson workup
Free copper (calculated)>15mcg/dLStop GHK-Cu, get 24-hour urinary copper
24-hour urinary copper>40mcg/dayStop GHK-Cu, hepatology referral

The free copper formula is the most useful single marker but it has a documented reliability problem. Duncan et al., 2017 showed substantial interlaboratory variability in the calculation, including frequent negative values when ceruloplasmin is measured immunologically rather than enzymatically. The formula is most reliable when ceruloplasmin is measured by enzymatic assay. If you get a negative free copper, the lab method, not your bloodwork, is the problem. Ask for a 24-hour urinary copper to confirm.

Week 12 (the honest readout)

Repeat the full panel. Add 24-hour urinary copper if not done at baseline. If you're stacking with CJC-1295 + ipamorelin or any GH secretagogue, add IGF-1 to track GH axis response (GLOW alone shouldn't move IGF-1).

The week 12 panel is your cycle-end checkpoint. If serum copper has crept into the 140-150mcg/dL range and free copper is trending up, you've answered the question of whether chronic GHK-Cu accumulates in your particular biology. That answer beats any vendor protocol.

The copper accumulation question, honestly

No published human study has measured serum copper or ceruloplasmin response to subcutaneous GHK-Cu injection. Every protocol you've read is theoretical extrapolation from copper toxicology and Wilson's disease literature. The arithmetic is solid:

  • GHK-Cu is 15.8% copper by mass
  • 50mg GHK-Cu vial contains 7.9mg elemental copper
  • Daily 2mg dose delivers 316mcg elemental copper systemically
  • 8-week daily cycle = 17.7mg cumulative copper injected, bypassing intestinal regulation
  • 12-week daily cycle = 26.6mg

For comparison, the oral Tolerable Upper Intake Level is 10mg/day, set on hepatotoxicity grounds. Chronic high-dose oral copper supplementation has been linked to drug-induced liver injury in the literature (LiverTox). The injected GLOW dose is well below those numbers on a per-day basis, but the route bypasses the gut, which means GHK-Cu is the most efficient copper-delivery vehicle most athletes will ever use.

The mechanism is what GHK-Cu was built for. Pickart originally proposed in 1973 that GHK functions as a copper-delivery carrier into cells via histidine and glycine coordination. The copper is supposed to be bioavailable. Topical and dermal absorption at cosmetic doses (0.2-2% creams) has a 40-year safety record. Daily subcutaneous injection at 2-3mg/day has zero years of safety record, because no one has studied it.

The Wilson's disease lab thresholds are the closest tool we have. They were developed for the opposite problem (genetic copper underclearance), but the markers (serum Cu, ceruloplasmin, free Cu, 24-hour urinary Cu) are the right ones for tracking copper status. The thresholds are conservative, which is the right call when nobody knows what "long-term safe" looks like for injected copper-peptide complexes.

Running GLOW on TRT or AAS

If you're on TRT alone, the bloodwork interpretation is straightforward. GLOW adds copper-peptide complexity to a stable hormonal baseline. The TRT panel you already run (total testosterone, free T, estradiol, SHBG, haematocrit) doesn't change. You add the GLOW panel on top.

The decision tree gets interesting when you stack GLOW with AAS, especially 17-alpha-alkylated orals like Dianabol, Anadrol, or Halotestin. Those compounds cause cholestatic liver injury with characteristic ALT, AST, GGT, and bilirubin elevation. BPC-157, in rats, prevents this kind of hepatic injury. In humans, we have no data.

So if ALT is up on your GLOW + AAS stack, here's the order of operations:

  1. Recheck with GGT and total bilirubin within 2 weeks. If GGT is also up, hepatic origin is confirmed. If GGT is normal, the elevation is likely from training or AAS-induced myocyte leak (not the liver). Continue cautious.
  2. If hepatic and bilirubin is under 2x ULN: blame the oral AAS. The prior probability is overwhelmingly higher than peptide-induced hepatic injury. Drop the oral dose by 50% or discontinue. Hold the peptide is unnecessary. Recheck in 2 weeks.
  3. If hepatic and bilirubin is over 2x ULN: stop the oral immediately. This is the classic cholestatic pattern from 17-alpha-alkylated compounds. You can continue the peptide if you want (no evidence of harm), but recheck weekly until things normalize.
  4. If ALT is over 5x ULN or bilirubin is over 3x ULN: stop everything injectable and oral. Get a hepatology consult. Don't try to figure it out yourself.
  5. The peptide is almost never the cause. Hold the peptide only if you've stopped the oral and ALT is still rising, you suspect contaminated product, or you want to isolate variables for diagnostic clarity.

For the full AAS hepatotoxicity baseline, the VitalMetrics liver enzymes on steroids article has the compound-by-compound risk hierarchy.

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GLOW for women on TRT

Most GLOW protocols and most peptide content is written for 80-100kg male users. Women, even on TRT, are not just smaller versions of that population. There are three real considerations:

Bodyweight scaling matters more. A 50kg woman on the default 2mg GHK-Cu dose receives 6.3mcg of copper per kg of body weight per day. A 100kg man on the same dose receives 3.2mcg/kg. Over an 8-week cycle, the woman's cumulative copper load per kg of lean body mass is roughly double the man's. Start at 0.05-0.07mL daily, not the standard 0.1mL.

Pregnancy is an absolute contraindication. BPC-157 upregulates VEGF and angiogenesis. TB-4 is a developmentally active peptide central to cardiogenesis. GHK-Cu modulates over 4,000 genes including proliferation pathways. None of the three have any human reproductive or teratology data. Women of childbearing potential should confirm non-pregnancy before starting and use contraception throughout. Stop immediately if pregnancy is suspected.

Iron status is more variable. Premenopausal women have menstrual iron loss, which affects ferritin and serum iron readings. Iron and copper interact metabolically, so a copper monitoring panel without paired iron studies can miss interactions. Run the standard iron panel (ferritin, serum iron, TIBC, transferrin saturation) alongside the copper panel at baseline and week 12.

The "menstrual cycle timing" recommendations that some practitioners give (pause peptide injections during menses) have no clinical evidence. It's preference, not pharmacology. If you want to follow it, fine. If you don't, fine.

GLOW vs running BPC-157 + TB-500 + GHK-Cu separately

Every informed user eventually asks this. The tradeoff is real and the answer is not "always GLOW" or "always separate."

The case for GLOW:

  • One vial, one reconstitution, one injection per dose event
  • Vendor convenience premium of $0.50-1/mg, but the time saved is real if you're already injecting TRT 1-2x/week
  • Eliminates the math errors that happen across three different reconstitution calculations
  • If you trust your vendor's QC, the 5:1:1 ratio is locked, which is one less thing to think about

The case for separate:

  • Ratio flexibility: titrate components independently. If serum copper is climbing at week 8, you can pause GHK-Cu alone while continuing BPC-157 and TB-500. GLOW locks you in.
  • QC distribution: three components from three tier-1 vendors hedges contamination risk. With GLOW, a single bad batch contaminates all three peptides simultaneously.
  • Storage stability: GHK-Cu is the limiting factor in any combined vial. It's sensitive to light and oxidizes faster than BPC-157 or TB-500. If your GLOW vial turns from blue to teal, all three peptides are compromised. Separate vials degrade independently.
  • Cost: separate components from tier-1 vendors with COAs typically run $0.67-2.54/mg vs GLOW's $1.14-2.14/mg. 20-40% cheaper for the same total peptide mass, with the same QC level.

The 5:1:1 ratio itself is vendor convention, not clinical evidence. There is no published human trial of GLOW or any BPC-157 + TB-500 + GHK-Cu combination, in any species. The ratio appears to have been empirically chosen by early biohackers and replicated by vendors because it sells. That's not a reason to avoid it. It's a reason not to treat it as optimized.

For an athlete already doing bloodwork and tracking copper, separate peptides give you more levers to pull when the data tells you something. For an athlete who wants the simplest possible protocol and trusts a specific vendor, GLOW is fine. For anyone uncertain, separate peptides offer better risk distribution at the cost of more logistics.

Cycle length and tapering

The dominant vendor protocol is 8 to 12 weeks on, 4 to 8 weeks off. PeptideFox uses a 3-phase frequency taper (daily for 4 weeks, then 5 times per week for 4 weeks, then 2-3 times per week for maintenance). None of this is clinically validated. There is no published trial that establishes an optimal cycle length, taper schedule, or wash-out interval for GLOW or any of its components.

The mechanistic case for cycling is weak. BPC-157's receptor target is not fully characterized, so tachyphylaxis can't be predicted but also can't be ruled out. TB-4 acts on G-actin (a structural protein, not a GPCR), so classical receptor desensitization is unlikely. GHK-Cu modulates gene expression through a different mechanism entirely. The "rotation principle" that's borrowed from GHRH and GHRP secretagogue protocols (where ghrelin receptor desensitization is well-documented) does not transfer cleanly to healing peptides.

The defensible case for cycling is exposure limitation, not pharmacology. Capping cumulative exposure of an under-studied compound is harm-reduction. Bloodwork checkpoints at washout give you actionable data: did serum copper return to baseline during the off-period? Did ferritin recover? Did hs-CRP move? Those are real reasons to cycle. "Avoiding receptor downregulation" is not.

For injury-specific use cases (post-op recovery, acute tendon repair), a time-limited block of 6-8 weeks tied to the recovery timeline is more defensible than open-ended chronic use. For aesthetic or general recovery use, 8-12 week blocks with full bloodwork at start and end is a reasonable harm-reduction default.

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What this article cannot tell you

Three things you should know about that are not in the published literature:

  1. Whether daily subcutaneous GHK-Cu raises serum copper measurably in humans. No PK study has been published. The arithmetic predicts accumulation; the biology might or might not confirm it.
  2. Whether BPC-157 lowers hs-CRP, ALT, or any inflammatory marker in athletes. Rat models say yes. Human data is one 2-person IV pilot at 20mg (Lee & Burgess, 2025) showing no measurable biomarker change.
  3. Whether the 5:1:1 GHK-Cu:BPC-157:TB-500 ratio is optimal for anything. It is vendor convention, not validated by any clinical trial.

When the literature is this thin, run your own bloodwork at fixed checkpoints and treat yourself as a single-subject experiment. The panel above gives you the data to do that. Two cycles in, you'll know what GLOW actually does to your bloodwork. Vendor copy will never give you that answer.

Track your GLOW bloodwork in one place

Log your baseline, week 4, and week 12 panels in VitalMetrics. Trend serum copper, ceruloplasmin, free copper, hs-CRP, and liver enzymes. Spot the drift before it becomes a problem.

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Key takeaways

  • A GLOW vial contains 50mg GHK-Cu, 10mg BPC-157, and 10mg TB-500 at a fixed 5:1:1 ratio. The 2mg GHK-Cu standard draw also delivers 400mcg BPC-157, 400mcg TB-500, and 316mcg of elemental copper subcutaneously.
  • An 8-week daily cycle injects ~17.7mg of cumulative elemental copper, bypassing intestinal regulation. The oral Tolerable Upper Intake is 10mg/day. No human study has measured serum copper response to chronic subcutaneous GHK-Cu.
  • The bloodwork panel: ALT, AST, GGT, bilirubin, hs-CRP, ferritin, albumin, serum copper, ceruloplasmin, calculated free copper. Run at baseline, week 4, week 12. Add 24-hour urinary copper if budget allows.
  • Bodyweight-titrated dosing: 50kg users at 0.05-0.07mL daily, 70-85kg at the default 0.1mL, 90-110kg at 0.12-0.15mL. The fixed 0.1mL draw is supratherapeutic for small users and subtherapeutic for large ones.
  • If ALT is up on a GLOW + AAS stack, the steroid is the cause until proven otherwise. The peptide is almost never the source of liver injury in this scenario.
  • For women: start at half the default draw, never use during pregnancy or lactation, pair copper with iron studies because of menstrual iron variability.
  • GLOW vs separate: separate peptides offer independent titration, QC distribution, and 20-40% lower cost. GLOW offers convenience and a locked ratio.
  • The 5:1:1 ratio is vendor convention. No published human trial validates it. Treat any GLOW cycle as a single-subject experiment with bloodwork as the readout.
Bruno Souza

Bruno Souza

IFBB competitor and founder of VitalMetrics. Passionate about harm reduction and helping athletes make informed decisions through bloodwork monitoring.

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References

  1. Pickart, L., & Thaler, M. M. (1973). Tripeptide in human serum which prolongs survival of normal liver cells and stimulates growth in neoplastic liver. Nature New Biology, 243(124), 85-87. PubMed

  2. Maquart, F. X., Pickart, L., Laurent, M., Gillery, P., Monboisse, J. C., & Borel, J. P. (1988). Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Letters, 238(2), 343-346. PubMed

  3. Sikiric, P., Seiwerth, S., Grabarevic, Z., Rucman, R., Petek, M., Jagic, V., Turkovic, B., Rotkvic, I., Mise, S., & Zoricic, I. (1993). Hepatoprotective effect of BPC 157, a 15-amino acid peptide, on liver lesions induced by either restraint stress or bile duct and hepatic artery ligation or CCl4 administration. Life Sciences, 53(18), PL291-296. PubMed

  4. Sikiric, P., Seiwerth, S., Rucman, R., Turkovic, B., Rokotov, D. S., Brcic, L., Sever, M., Klicek, R., Radic, B., Drmic, D., Ilic, S., Kolenc, D., Stambolija, V., Zoricic, Z., Vrcic, H., & Sebecic, B. (2014). Stable gastric pentadecapeptide BPC 157-NO-system relation. Current Pharmaceutical Design, 20(7), 1126-1135. PubMed

  5. Pickart, L., Vasquez-Soltero, J. M., & Margolina, A. (2018). Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. International Journal of Molecular Sciences, 19(7), 1987. PubMed

  6. Mazurowska, L., & Mojski, M. (2007). ESI-MS study of the mechanism of glycyl-L-histidyl-L-lysine-Cu(II) complex transport through model membrane of stratum corneum. Talanta, 72(2), 650-654. PubMed

  7. Hostynek, J. J., Dreher, F., & Maibach, H. I. (2011). Human skin penetration of a copper tripeptide in vitro as a function of skin layer. Inflammation Research, 60(1), 79-86. PubMed

  8. Lee, E., & Burgess, J. (2025). Safety of intravenous infusion of BPC-157 in humans: A pilot study. Alternative Therapies in Health and Medicine. PubMed

  9. Ruff, D., Crockford, D., Girardi, G., & Zhang, Y. (2010). A randomized, placebo-controlled, single and multiple dose study of intravenous thymosin beta4 in healthy volunteers. Annals of the New York Academy of Sciences, 1194(1), 223-229. PubMed

  10. Sosne, G., Dunn, S. P., & Kim, C. (2015). Thymosin beta4 significantly improves signs and symptoms of severe dry eye in a phase 2 randomized trial. Cornea, 34(5), 491-496. PubMed

  11. Goldstein, A. L., Hannappel, E., Sosne, G., & Kleinman, H. K. (2012). Thymosin beta4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opinion on Biological Therapy, 12(1), 37-51. PubMed

  12. Esposito, S., Deventer, K., Geldof, L., & Van Eenoo, P. (2012). Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential. Drug Testing and Analysis, 4(9), 733-738. PubMed

  13. Roberts, E. A., & Schilsky, M. L. (2008). Diagnosis and treatment of Wilson disease: an update. Hepatology, 47(6), 2089-2111. PubMed

  14. Walshe, J. M. (2003). Wilson's disease: the importance of measuring serum caeruloplasmin non-immunologically. Annals of Clinical Biochemistry, 40(Pt 2), 115-121. DOI

  15. Duncan, A., Yacoubian, C., Beetham, R., Catchpole, A., & Bullock, D. (2017). The role of calculated non-caeruloplasmin-bound copper in Wilson's disease. Annals of Clinical Biochemistry, 54(6), 649-654. PubMed

  16. Institute of Medicine. (2001). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press. Chapter on Copper. NCBI Bookshelf

  17. National Institutes of Health, LiverTox. (2020). Copper. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. NCBI Bookshelf

  18. He, L., Feng, D., Guo, H., Zhou, Y., Li, Z., Zhang, K., et al. (2022). Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs. Frontiers in Pharmacology, 13, 1026182. DOI

  19. Hsieh, M. J., Liu, H. T., Wang, C. N., Huang, H. Y., Lin, Y., Ko, Y. S., et al. (2017). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of Molecular Medicine, 95(3), 323-333. PubMed

  20. Wang, S., et al. (2021). A first-in-human, randomized, double-blind, single- and multiple-dose, phase I study of recombinant human thymosin beta4 in healthy Chinese volunteers. Journal of Cellular and Molecular Medicine, 25(17), 8466-8479. PubMed

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