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Thymulin (FTS)9 residues (approx.)QAKSQGGSNEach bubble = one amino acid. Size = residue mass. Color = chemical class.Uses closest standard amino acids for non-standard residues.Also known as: FTS, Serum Thymic Factor, Thymic Factor
Nine amino acids and one zinc ion. That's the entire molecule behind thymulin, a thymic hormone your body stops producing in detectable amounts by age 60. Reggiani and colleagues mapped its physiology and therapeutic potential in a 2014 review [1], confirming that this nonapeptide drives T-cell differentiation through a zinc-dependent conformational switch that no other thymic peptide shares. Community use sits in niche territory, with protocols built around short 10 to 20 day courses rather than continuous dosing. The catch: only one human interventional trial exists, and it dates back to 1982.
Your thymus quietly stops making thymulin somewhere around middle age. By 60, circulating levels are often undetectable, and that decline tracks closely with the immune erosion that comes with aging. Thymulin, also called Facteur Thymique Serique (FTS) or Serum Thymic Factor, is a nonapeptide (pGlu-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn) with a molecular weight of 858.9 Da and a CAS number that reflects its metallopeptide nature. The mechanism is unusual. Without zinc, thymulin circulates as a biologically inert apoform. One zinc ion locks the peptide into a three-dimensional shape that can actually bind T-cell receptors and trigger differentiation cascades. Dardenne and colleagues characterized this zinc dependency in 1989 [2]; NMR work later confirmed the specific coordination through Lys3, Ser4, and the Ala2 backbone carbonyl. In animal models, thymulin administration reduced TNF-alpha, IL-1beta, and IL-6 through NF-kB inhibition (Lunin and Novoselova 2008)[3]. A colitis mouse model showed measurable anti-inflammatory effects at 15 mcg per 100g body weight (Lunin and Bhatt 2007)[4]. T-cell maturation markers shifted, NK cell activity improved, and Hsp70 overproduction dropped. The human evidence gap is real. Bordigoni and colleagues ran one interventional trial in immunodeficient children in 1982, published in the Lancet. That trial has not been replicated in over 40 years. All adult dosing comes from animal study extrapolation and practitioner experience. Thymulin sits in emerging research territory with a strong mechanistic foundation but no validated human dose-ranging data for healthy adults.
Thymulin's activation depends on a single zinc ion. The inactive apoform circulates freely in plasma but can't do anything useful until zinc coordinates through the side chains of Lys3 and Ser4 and the backbone carbonyl of Ala2. That metalation event changes the peptide's three-dimensional structure, exposing an epitope that T-cell surface receptors recognize. Coto and colleagues reviewed this zinc-thymulin interaction in detail [5]. Once the active zinc-bound form binds T-cell precursors, intracellular cAMP signaling kicks off differentiation. Maturation markers including CD4, CD8, and the T-cell receptor complex increase in expression. In mature T cells, thymulin boosts IL-2 production, allogenic cytotoxicity, and suppressor cell function. The anti-inflammatory arm runs through NF-kB. Thymulin blocks nuclear localization of NF-kB via the IkB-alpha/pIkB-alpha pathway. Safieh-Garabedian and colleagues confirmed this is the primary anti-inflammatory mechanism. Downstream, transcription of TNF-alpha, IL-1beta, and IL-6 drops while anti-inflammatory IL-10 stays intact or increases. Zinc amplifies this effect synergistically. Intracerebroventricular administration in animal models reduced hippocampal NF-kB activation and attenuated neuroinflammatory damage; thymulin also prevented LPS-induced Hsp70 overproduction [3]. These findings point to neuroprotective potential, though all of this work remains preclinical.
Animal and in vitro evidence strongly supports T-cell differentiation, NK cell activation, and NF-kB-mediated anti-inflammatory effects. Zinc dependency is mechanistically confirmed by NMR. Only one human interventional trial exists (Bordigoni 1982, Lancet, immunodeficient children: never replicated). No dose-ranging human studies in healthy adults.
Reggiani et al. 2014 (PMID 24588820): best available review of physiology and therapeutic potential; Bordigoni et al. 1982 (Lancet): only human interventional trial; Lunin & Bhatt 2007 (PMID 17499195): anti-inflammatory colitis model
Zero human dose-ranging trials in healthy adults. Sole human interventional trial from 1982 in immunodeficient pediatric patients, never replicated in 44 years. All adult dosing is extrapolated from animal studies or practitioner experience. Mechanism is well-established; efficacy and safety in healthy adults are unproven.
Niche use among longevity-focused biohackers and immune optimization practitioners. Used in short intensive courses (10–20 days) targeting immunosenescence and T-cell support. Very low discussion volume: primarily practitioner and vendor protocol driven, not grassroots community.
Mechanism alignment is strong: both science and community agree on zinc dependency, T-cell differentiation effects, and anti-inflammatory activity via NF-kB. Dosing is not aligned: animal studies use mcg/kg, the one human trial used pediatric immunodeficient patients, and community protocols use mg/day flat dosing for healthy adults with no clinical basis. Course structure also diverges: 10–20 day intensive courses in community vs. continuous weekly dosing implied by current site tiers.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 50mcg | 2x/week |
| Moderate | 100mcg | 3x/week |
| Aggressive | 200mcg | Daily |
Thymulin won't do anything without zinc on board. Start 15 to 30 mg elemental zinc daily at least 7 days before your first injection. Zinc citrate or bisglycinate absorb better and cause less stomach upset than zinc oxide. Reconstitution math for a 5 mg vial: add 2.5 mL bacteriostatic water to get 2 mg per mL. For the beginner 2 mg dose, draw 1 mL (100 units on a U-100 insulin syringe). For a 5 mg intermediate dose, reconstitute a 5 mg vial with 1 mL BAC water to get 5 mg per mL; draw 1 mL (100 units). The single biggest mistake in this space is confusing thymulin with thymalin. Thymulin is one defined 9-amino-acid peptide, MW 858.9 Da. Thymalin is a heterogeneous polypeptide extract from calf thymus. They are structurally different compounds with different evidence bases. Always verify the COA confirms molecular weight of 858.9 Da before your first dose. The 10-minute serum half-life means daily dosing is non-negotiable. Protocols using 2 to 3 times per week are almost certainly subtherapeutic. Short intensive courses (10 to 20 days) make more pharmacokinetic sense than stretched-out weekly schedules.
No standardized human cycling protocols exist. The 8-on/4-off recommendation is based on animal study durations and the general principle of allowing immune system recalibration between treatment periods. Zinc supplementation (15-30 mg/day elemental zinc) should begin 1 week before starting thymulin and continue throughout the cycle. Monitor zinc and copper levels during extended use, as chronic zinc supplementation can deplete copper stores.
No long-term human safety data exists for continuous exogenous thymulin administration. Short intensive courses (10–20 days, 3x/year) are modeled on animal study durations and align with natural pulsatile thymic hormone biology. The ~10-minute serum half-life makes sustained therapeutic plasma levels pharmacologically impossible via conventional injection: supporting burst-dosing courses over continuous use. NOTE: The current peptides.ts cyclingProtocol (onWeeks: 8, offWeeks: 4) has no basis in any published or community source; the 10–20 day intensive course model is the universal standard.
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Expected: T-cell modulation beginning around days 7–10 based on animal study timelines. Possible subjective reduction in minor illness frequency over following 2–3 months. Anti-inflammatory effects expected by end of course. No dramatic short-term perceptible changes anticipated.
Monitor: Check serum zinc before starting (target 70–120 mcg/dL). Monitor copper at baseline and after 2+ consecutive cycles: chronic zinc supplementation depletes copper.
You should have taken 15 to 30 mg elemental zinc daily for at least 7 days before this first injection. Test serum zinc if possible (target above 70 mcg per dL).
Add bacteriostatic water slowly down the inside wall. For a 5 mg vial at the beginner 2 mg dose, add 2.5 mL BAC water (2 mg per mL concentration). Swirl gently. Never shake.
For 2 mg at 2 mg per mL concentration, draw to the 100 unit mark on a U-100 insulin syringe. For a 5 mg dose reconstituted at 5 mg per mL, also draw to 100 units. For the advanced 10 mg dose, reconstitute a 10 mg vial with 2 mL BAC water (5 mg per mL); draw 2 mL total, split into two separate 1 mL (100 unit) injections at different sites.
Inject subcutaneously into abdominal fat using a 29 to 31 gauge needle, half-inch length. Pinch a fold of skin, insert at a 45 degree angle, inject slowly.
Morning dosing at a consistent time is the standard protocol.
If running two or more consecutive cycles, add 2 mg copper bisglycinate daily, taken at least 2 hours apart from zinc.
Store reconstituted vials upright in the refrigerator at 2 to 8 degrees Celsius. Use within 14 days. Do not freeze reconstituted solution.
Most common thymulin stack. TA1 promotes Th1 differentiation and antiviral immunity via TLR/MAPK pathways with 40+ human trials; thymulin adds direct T-cell maturation via zinc-dependent cAMP signaling. Complementary mechanisms with no known interaction risk.
Run concurrently: thymulin 2–5 mg daily SC (course duration) + TA1 1.5 mg SC 2x/week. Overlap timing if running separate course lengths.
Longevity pairing combining thymulin's T-cell/anti-inflammatory effects with Epithalon's telomerase activation and pineal/circadian benefits. Common in immunosenescence-focused protocols targeting multiple aging pathways simultaneously.
Sequential or overlapping courses: Epithalon 5–10 mg daily SC × 10 days, then thymulin 2–5 mg daily SC × 20 days.
Combines thymulin's adaptive immunity (T-cell maturation) with LL-37's innate immune coverage (antimicrobial, neutrophil and macrophage activation). Community-reported for broad immune defense pairing.
Anti-inflammatory synergy: KPV inhibits NF-kB via MC1R/alpha-MSH receptor; thymulin inhibits NF-kB via cAMP/IkB-alpha phosphorylation. Two different mechanistic entry points into the same pro-inflammatory pathway: additive anti-inflammatory coverage without known interaction.
Thymulin activates T-cell proliferation and NK cell activity: directly opposing immunosuppressive therapy goals. High risk of transplant rejection or immune-mediated organ damage in transplant patients.
Do not combineBoth thymulin and checkpoint inhibitors amplify T-cell activation via different mechanisms. Combined effect is entirely unstudied. Unpredictable T-cell hyperactivation and immune-related adverse events are a theoretical concern.
Do not combineNot inherently dangerous to combine, but thymalin (heterogeneous polypeptide thymic extract) is frequently substituted for thymulin (single defined nonapeptide, MW 858.9 Da) by vendors and buyers. Verify compound identity via COA before ordering. Do not stack without confirming you have the correct compound.
Pricing updated 2026-04-09
The most serious concern with thymulin is the total absence of long-term human safety data for exogenous administration in healthy adults. One interventional trial exists (Bordigoni et al. 1982, Lancet, immunodeficient children), and it has never been replicated. Every side effect profile below comes from animal studies, limited clinical observation, and practitioner reports from a very small user base. Autoimmune flare is the highest-stakes risk. Thymulin directly activates T-cell proliferation and NK cell function. Anyone with an active autoimmune condition, a history of autoimmune episodes, or an organ transplant on immunosuppressive therapy should not use this peptide. T-cell activation in those populations can trigger graft rejection or worsen immune-mediated tissue damage. This is not a theoretical concern; it is a pharmacological certainty based on thymulin's mechanism. Copper depletion is the most commonly missed long-term risk. Thymulin requires continuous zinc supplementation (15 to 30 mg per day) to remain biologically active. Chronic zinc intake at those levels competitively inhibits copper absorption. Over multiple cycles, copper deficiency produces fatigue, anemia, brittle nails, and hair loss. These symptoms directly undermine the reason you started thymulin in the first place. Monitor serum copper and ceruloplasmin at baseline and after every two consecutive cycles. Add 2 mg per day copper bisglycinate, separated from zinc by at least two hours. Some users report transient fatigue during the first few days of a course. Community reports describe this as immune recalibration. It typically self-resolves by day 5 to 7. Reducing the dose by 50 percent is reasonable if fatigue becomes debilitating. Injection site reactions (redness, mild discomfort) are standard for subcutaneous peptides and don't require intervention beyond site rotation. Rare reports include headache and nausea. No dose-dependent adverse event data exists in humans. The mcg versus mg dosing confusion is a safety issue, not just a practical one. Community protocols use mg (2 to 10 mg per day). Scientific animal literature reports doses in mcg per kg. A misread produces a 1,000-fold error in either direction. Always verify units before reconstitution. Active cancer without oncologist clearance is a contraindication. T-cell and NK cell activation may interact unpredictably with tumor biology. Pregnancy and breastfeeding are absolute contraindications; no reproductive safety data exists. Wilson's disease or copper metabolism disorders add extra risk because the mandatory zinc supplementation further disrupts copper balance. Stop immediately and seek medical evaluation if you develop joint pain, unexplained rash, persistent fever above 38.5 degrees Celsius, or lymphadenopathy during a course.
Verify Thymulin (FTS) dosing and safety with a second opinion
Thymulin and thymalin are structurally distinct compounds (single nonapeptide vs. heterogeneous polypeptide extract) that are frequently confused at the vendor and buyer level: documented mislabeling is a real risk. No pharmaceutical-grade thymulin exists and no compounding pharmacy programs are available. Research compound with no pharmacopoeial standard or FDA oversight. The mcg/mg dosing unit confusion compounds quality and safety risk.
| Test | When | Target |
|---|---|---|
| Serum Zinc | Before starting zinc pre-load; again at 2 weeks into first course | 70–120 mcg/dL |
| Serum Copper + Ceruloplasmin | At baseline; monthly during extended use (2+ consecutive cycles); 4 weeks post-course | Copper: 70–140 mcg/dL; Ceruloplasmin: 20–60 mg/dL |
| CBC with Differential (lymphocyte subsets: CD3/CD4/CD8/CD56) | At baseline; 4–6 weeks after completing course | CD4:CD8 ratio 1.5–2.5; total lymphocyte count within laboratory reference range |
| High-sensitivity CRP + IL-6 | At baseline; 4–6 weeks post-course | hsCRP < 3 mg/L; IL-6 < 7 pg/mL |
Thymulin is biologically inactive without adequate zinc. Baseline deficiency renders the peptide ineffective regardless of dose. Post-pre-load test confirms repletion was achieved.
Chronic zinc supplementation required for thymulin activity competitively inhibits copper absorption. Copper deficiency causes fatigue, anemia, and immune impairment: directly undermining the goal of thymulin use. This is the most commonly missed monitoring requirement.
Objective measure of T-cell population changes. CD4/CD8 ratio shifts and total lymphocyte counts confirm biological response. Also detects unexpected lymphopenia or lymphocytosis.
Primary markers of thymulin's anti-inflammatory mechanism. Both CRP and IL-6 are downstream of NF-kB activation, which thymulin suppresses via IkB-alpha phosphorylation. Post-course reduction confirms response.
Treatment initiation alongside zinc pre-loading. Thymulin begins interacting with T-cell precursors. No outward immune changes expected during this window. Mild injection site reactions may occur. Ensure zinc supplementation is consistent.
Early T-cell modulation may begin. In animal studies, thymulin administration during this timeframe produced measurable changes in T-cell subpopulations and cytokine profiles. Some individuals report subtle improvements in energy or reduced frequency of minor infections.
Anti-inflammatory effects become more established. In colitis mouse models, thymulin at 15 mcg/100g body weight significantly reduced pro-inflammatory cytokine accumulation in this timeframe. T-cell maturation markers and NK cell activity may show improvement on blood panels.
Peak treatment effects expected. Immune rebalancing is most apparent with sustained use. Assess results through bloodwork (T-cell subsets, inflammatory markers). Evaluate whether to continue another cycle after the off-period.
Days negative 7 to 0 (Zinc Pre-Load): Start zinc supplementation before touching thymulin. A 2025 Immunity and Ageing study confirmed that 20 mg per day zinc for 16 weeks increased circulating active thymulin levels, particularly in lean individuals. Zinc repletion makes or breaks this entire protocol. Some users notice improved energy or sleep just from correcting a zinc deficit. Expect mild GI upset if you take zinc without food. Days 1 through 7 (Week 1): Zinc-bound thymulin starts binding T-cell receptors and activating cAMP signaling. NF-kB nuclear localization begins to be suppressed. You won't feel immune changes yet. Some users experience transient fatigue during the first few days as immune populations shift. Injection site redness is possible. Rare headache. Days 7 through 20 (Weeks 2 to 3): This is where the animal data gets interesting. Lunin's 2007 colitis model [4] showed measurable TNF-alpha, IL-1beta, and IL-6 reductions in colon tissue by days 10 to 20 at 15 mcg per 100g body weight. T-cell maturation markers and NK cell activity shift. Hsp70 overproduction drops [3]. Older users (50+) are most likely to notice subtle changes; younger users rarely report anything acute during the course itself. If you develop joint pain, rash, or fever, stop immediately and evaluate for autoimmune activation. 4 to 8 weeks post-course: The assessment window. T-cell population changes may persist for weeks after the course ends in animal models. Bloodwork is the only objective readout: T-cell subsets (CD3, CD4, CD8, CD56), CRP, IL-6. Most users track outcomes by monitoring illness frequency over the following 2 to 3 months. Those stacking with Thymosin Alpha-1 tend to attribute results to the combination rather than thymulin alone.
Zinc repletion ensures thymulin can adopt its active metallopeptide conformation from day 1. A 2025 Immunity & Ageing study found 16 weeks of 20 mg/day zinc significantly increased circulating active thymulin levels, particularly in lean individuals: confirming zinc is a rate-limiting co-factor for both endogenous and exogenous thymulin activity.
No immune changes attributable to thymulin. Some users report improved energy or sleep from zinc repletion alone if baseline zinc was low. No injection site issues.
Zinc-bound thymulin begins binding to high-affinity T-cell surface receptors. cAMP signaling initiates differentiation cascades. NF-kB nuclear localization starts to be downregulated, beginning to reduce pro-inflammatory cytokine transcription (TNF-alpha, IL-1beta, IL-6).
No perceptible immune changes expected. Mild injection site redness is possible. ~25–35% of users experience transient fatigue from day 2–5 as immune recalibration begins.
Mouse colitis data (Lunin 2007, 15 mcg/100g BW) showed measurable reductions in TNF-alpha, IL-1beta, and IL-6 in colon tissue by day 10–20. T-cell maturation markers (CD4, CD8) and NK cell activity expected to shift. Hsp70 overproduction suppressed (Lunin 2008, PMID 18991101).
Older users (50+) most likely to notice subtle subjective changes. Younger users rarely report acute perceptible differences during the course. Anti-inflammatory benefit is most apparent in users with elevated baseline inflammatory markers.
T-cell population changes may persist for weeks post-course in animal models. Bloodwork (T-cell subsets, CRP, IL-6) is the objective readout. Circulating thymulin levels decline with age and are often undetectable by 60: post-course benefit depends partly on residual endogenous production.
Most users assess outcomes by tracking illness frequency over the following 2–3 months. Few report dramatic subjective changes when thymulin is used alone vs. stacked with TA1. Users stacking with TA1 typically attribute combined benefits to the combination rather than thymulin alone.
Source: Serum half-life of thymulin is approximately 10 minutes based on clearance studies. This extremely short duration is one of the primary pharmacokinetic limitations, and gene therapy approaches have been explored to achieve sustained endogenous production. Circulating levels in healthy humans range from 0.5-3 pg/mL, peaking in early childhood and becoming undetectable by age 60.
Loading the interactive decay curve.
Thymulin is classified as a research compound. It has no FDA approval for any indication and is not available through compounding pharmacies. Purchase is restricted to "for research purposes only" through peptide research suppliers. No pharmaceutical-grade formulation exists, and there is no pharmacopoeial standard or monograph. WADA status should be verified by competitive athletes before use, as thymic peptides and immunomodulators may fall under prohibited substance categories depending on the sport and testing body. No pending regulatory actions or scheduled FDA reviews are publicly documented for thymulin as of early 2026. The gene therapy research direction (adeno-associated viral vectors encoding thymulin) operates under entirely separate regulatory pathways from the synthetic peptide. This content is provided for educational and research purposes only. Thymulin is not approved for human therapeutic use. All dosing information is derived from animal studies and community protocols, not validated human clinical trials. Consult a qualified healthcare provider before using any research compound.
Peptide Schedule Research TeamReviewed Apr 20268 Citations
