ImmuneThymosin Alpha-1Thymosin α1

Thymosin Alpha-1

Tα1 / thymalfasin · thymic immunomodulatory peptide (Zadaxin)

Thymosin alpha-1 is a 28-amino-acid immune-signaling peptide — the N-terminal fragment of prothymosin alpha, first isolated from thymus extract in 1977. It is the rare catalog peptide with genuine large randomized trials and real regulatory approval abroad: as thymalfasin / Zadaxin it is nationally registered in roughly 35 countries (notably China and Italy) for chronic hepatitis B. It is NOT approved by the US FDA or centrally by the EU's EMA. The honest catch is that the best-quality recent evidence runs against the headline claims. The largest, most rigorous study — a 1,089-patient double-blind, placebo-controlled Phase 3 sepsis trial (2025) — found no survival benefit (hazard ratio 0.99), overturning an earlier, smaller, single-blind study that had looked marginally positive. The same 'collapses under rigor' pattern appears in COVID-19 (an apparent benefit vanished once researchers adjusted for who received the drug) and in a large melanoma trial (which missed statistical significance). Where the evidence is genuinely supportive, it is narrow: as an add-on in chronic hepatitis B, and for improving vaccine antibody responses in elderly or immunocompromised people. None of this supports the 'general immune-boosting,' anti-aging, or longevity use it is marketed for online — there are zero positive trials in healthy people for any wellness endpoint. In the US its compounding status is unresolved: placed on the FDA's 503A safety-risk list in 2023, then removed in 2024 only because the nomination was withdrawn, not because it was endorsed. This page documents what the primary trials actually show.

The short version

Thymosin alpha-1 is a small natural peptide — 28 amino acids long — that your thymus gland produces as part of how the body tunes its immune system. It was first isolated from thymus extract in 1977. The lab-made version is called thymalfasin, sold under the brand name Zadaxin. It works mainly by maturing dendritic cells — the immune system's 'scouts' — which in turn steer T-cells toward a particular kind of response.

Here is the unusual part for a peptide sold online: this is a real, approved medicine — but abroad. It is registered in roughly 35 countries (most prominently China and Italy) as a treatment for chronic hepatitis B. It is NOT approved by the US FDA, nor centrally by Europe's EMA.

And here is the honest catch. The best, most carefully run studies actually cut against the hype. The biggest, best-designed sepsis trial — over a thousand patients, properly blinded and placebo-controlled, published in 2025 — found that it did NOT save lives, overturning a smaller, weaker earlier study that had looked promising. The same thing happened with COVID-19 (it looked helpful in rough early data, but the benefit vanished once researchers accounted for which patients actually received it) and with a large melanoma trial (which just missed the bar for significance).

Where it genuinely seems to help is narrow and specific: added on to hepatitis B treatment, and boosting the antibody response to vaccines in elderly or immune-compromised people. None of that is the 'boost a healthy person's immune system,' anti-aging, or longevity use it is marketed for online — there is no good trial supporting that. On top of that, its US regulatory status is in limbo. This page lays out exactly what the real trials found, and where they stop.

Molecular identity

Specs

Molecular weight: 3108.3 g/mol (average)
Molecular formula: C129H215N33O55
Monoisotopic mass: 3106.5041 Da (exact mass 3107.5075)
PubChem CID: 16130571 (thymalfasin)

Sequence (28 AA): Ac-Ser-Asp-Ala-Ala-Val-Asp-Thr-Ser-Ser-Glu-Ile-Thr-Thr-Lys-Asp-Leu-Lys-Glu-Lys-Lys-Glu-Val-Val-Glu-Glu-Ala-Glu-Asn (N-terminally acetylated)PubChem CID 16130571
Structure / class: N-terminally acetylated 28-residue immunomodulatory peptide; N-terminal 1–28 fragment of prothymosin alphaPubChem CID 16130571; PMID 265536
Origin: Isolated 1977 from thymosin fraction 5 (Goldstein lab); synthetic form = thymalfasinPMID 265536
CAS / UNII: 62304-98-7 (also 69521-94-4) · W0B22ISQ1CPubChem / FDA UNII
Molecular target: No single receptor; immunomodulator acting on dendritic cells via TLR2/TLR9–MyD88 signaling → Th1 polarizationResearch literature
Half-life (human, SC): Under 3 h (primary study; commonly cited ~2 h); returns to baseline within 24 hPMID 10027483Half-life curve →
Regulatory status: NOT FDA-approved and NOT EMA-centrally approved; nationally registered as Zadaxin (thymalfasin) in ~35 countries for chronic hepatitis B; removed from FDA 503A Category 2 list in 2024 on a withdrawn nomination (not on Category 1)FDA / national drug registers

Plain English

Mechanism

Thymosin α1 is a 28-residue peptide corresponding to the N-terminal portion (residues 1–28, the front end of the chain) of prothymosin alpha, a larger nuclear precursor protein. Its N-terminal acetylation (a small chemical cap on that front end) is essential for full biological activity and is present in both the natural peptide and synthetic thymalfasin. It is an immunomodulator — something that adjusts immune signaling rather than acting as a hormone or a growth factor.

The clearest mechanistic work shows that Tα1 acts primarily on dendritic cells (the immune system's 'scouts' that decide what counts as a threat) rather than directly on T-cells (the immune system's attacking and coordinating cells). In cell-culture and mouse studies, it drives dendritic-cell maturation and interleukin-12 production (interleukin-12 being a signaling molecule that switches on aggressive immunity) through MyD88-dependent Toll-like receptor signaling — Toll-like receptors being the cell's pattern-recognition alarms, here TLR9 and TLR2 — promoting a Th1-polarized response (steering immunity toward the branch that fights viruses and intracellular bugs); for example, protective antifungal immunity in a mouse Aspergillus (a common mold) model. A complementary line of work shows it also engages dendritic-cell tryptophan catabolism (IDO — an enzyme pathway that breaks down the amino acid tryptophan), helping balance inflammation against tolerance. These are well-characterized findings, but they are largely in vitro (in lab dishes) and in animal models.

The clearest human mechanistic readout comes from sepsis (a life-threatening, body-wide reaction to infection): in the ETASS trial, Tα1 improved monocyte HLA-DR expression — a marker of reversing the immune 'paralysis' that sepsis induces (monocytes being frontline immune cells, and HLA-DR a surface tag that shows they are awake and working). Broader reported effects (enhancing T-cell maturation and NK-cell — natural killer cell — activity, raising Th1 cytokines, the chemical messengers of that virus-fighting branch, such as IFN-γ and IL-2, and reducing T-cell exhaustion markers like PD-1, a brake molecule that builds up on worn-out immune cells) come mostly from preclinical or disease-state studies and remain partly inferential in humans.

The honest mechanistic summary: Tα1 has a genuinely well-characterized immunomodulatory mechanism centered on dendritic cells and Toll-like receptor signaling, demonstrated mostly in vitro and in animals, with a human signal (mHLA-DR restoration) in sepsis. That a mechanism is real does not, by itself, make the clinical claims true — and as the trials below show, the rigorous outcome data are mixed-to-negative for the headline indications.

Sources:PubChem CID 16130571 PMID 265536 PMID 14982877 PMID 23327199

Why people reach for it

Potential benefits

Thymosin Alpha-1 is unusual for a catalog peptide — a real, foreign-approved drug with genuine trials. Here's what draws people to it, kept strictly to where the evidence actually points and away from the wellness claims it can't support.

A genuinely characterized immune mechanism — Unlike most research peptides, Thymosin Alpha-1 has a well-mapped mechanism — it matures dendritic cells through Toll-like receptor signaling and steers a Th1-polarized response, which is why it's taken seriously as an immune modulator.
Real evidence as a hepatitis-B add-on — Its strongest support is as an adjunct to antiviral therapy in chronic hepatitis B, where add-on trials reported higher viral-control markers — the basis for its approval abroad as Zadaxin.
Boosting vaccine response where it's weak — Studied as a vaccine co-adjuvant in elderly and immunocompromised people, it improved antibody titers in those who otherwise respond poorly — its most scientifically coherent wellness-adjacent use.
A clean short-term tolerability record — Across its studied uses the drug-related side-effect rate runs under 1%, mostly mild injection-site reactions — an unusually clean short-term safety picture within the populations and durations actually tested.
Approved medicine abroad, not a gray-market unknown — As thymalfasin it is nationally registered in roughly 35 countries for chronic hepatitis B — a real regulatory pedigree most peptides lack, even though it is not FDA-approved.

Sources:PMID 19467157 PMID 22010537 PMID 14982877 PMID 39814420

What people reach for Thymosin Alpha-1 for, drawn from what the trials actually report and how it's used — not proven outcomes or medical claims. Honest limits: the most rigorous trial (Phase 3 sepsis) was null, and there are zero positive trials in healthy people for general immune-boosting, anti-aging, or longevity.

Implied timing

Best time to dose

Implied best time

Anytime (consistent)

Most people take Thymosin Alpha-1 at a consistent time on its dosing days — it's an immunomodulator dosed a couple of times a week, not something tied to a specific hour.

Its action is immune signaling — dendritic-cell maturation and T-cell polarization build over days, not within a single dosing window — so no time of day is mechanistically favored.
The supportive trials dosed twice weekly without specifying a time; picking fixed days (e.g. Monday and Thursday) at a repeatable hour is the practical lever for adherence, which matters more than morning-versus-evening.
Its serum half-life is short (under 3 hours), so the dose doesn't linger and there's nothing to schedule around — consistency, not timing, is what keeps the twice-weekly rhythm intact.

No study establishes an ideal time of day for Thymosin Alpha-1 — this is reasoned from its mechanism and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for Thymosin Alpha-1 any consistent time on its dosing days is fine.

Sources:PMID 10027483

How to run it

Dosing & protocol

Thymosin α1 is dosed here as a subcutaneous injection — the only route studied in human trials (the Zadaxin label explicitly prohibits intravenous administration) and the route the on-page calculator is built for. Unlike most catalog peptides, the figures below come from real human trials in sick patients, not from animal extrapolation. That context changes how they should be read: no trial has ever tested a regimen in a healthy person, so there is no validated wellness, anti-aging, or immune-boosting schedule.

Real foreign-approved drug — but every studied dose was given to sick or vulnerable patients (hepatitis B, sepsis, cancer, vaccine non-responders). The largest, most rigorous trial (Phase 3 sepsis, n=1,089, double-blind) was null. There is no validated regimen for healthy-person use. Doses below are the trial-established schedules, not a recommendation.

Tiered dose ranges

The two trial shapes divide sharply by indication — the chronic outpatient pattern versus the acute inpatient pattern. The former is the only one with positive evidence.

Chronic / outpatient (hep-B, vaccine adjuvant):: 1.6 mg subcutaneously twice weekly — the Zadaxin-approved hepatitis-B dose, sustained over 6–12 months as an add-on to antiviral therapy. Vaccine-adjuvant studies used the same twice-weekly cadence over a short defined course (eight doses) in elderly or immunocompromised people. This is the dose with the narrowest but most supportive human evidence.
Acute / inpatient (sepsis — studied, but null):: Twice daily for 5 days then once daily for 2 days (the ETASS dose); or every 12 hours for 7 days (the TESTS Phase 3 dose). Both were short hospital-only courses for critically ill patients — not a standing outpatient pattern. The largest, most rigorous trial at this schedule was null (HR 0.99, p=0.93). Listed for completeness, not to emulate.

Subcutaneous administration

Thymosin α1 is injected subcutaneously; the Zadaxin label specifies this route and prohibits intravenous use. Site, timing, and food window are the actionable choices.

Injection site:: The abdomen (a couple of inches clear of the navel), the outer thigh, or the love-handle area. Rotate sites between doses — using the same spot repeatedly risks local irritation and fatty lumps (lipohypertrophy).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial; the reconstitution card below converts 1.6 mg to syringe units at the standard mix, and the on-page calculator handles any vial size.
Time of day:: No circadian timing data exists for Tα1, and it isn't time-locked. In the hep-B and vaccine trials, twice-weekly dosing was not time-specified — a consistent time on fixed days (e.g., Monday and Thursday) is the practical convention to build a repeatable habit. See Best time to dose above.
Food window:: Subcutaneous Tα1 does not interact with food absorption — it can be injected independently of meals.

Cycle & washout

The only trial-established cycle shapes are disease-specific. For off-label research use, community convention borrows from the outpatient hepatitis-B template.

Standard research cycle:: 6–12 weeks of twice-weekly dosing (mirroring the hepatitis-B trial cadence), then assess — checking relevant immune markers if available.
Washout:: A 4–8-week break before repeating. Tα1's serum half-life is short (under 3 hours), so accumulation is not the concern; the break is standard peptide-pulsing convention applied to an immunomodulatory agent.
No validated wellness cycle:: There is no evidence-backed cycle for general immune support, anti-aging, or longevity use in healthy people — this washout framing is practical convention, not a studied protocol.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for the default vial (10 mg, 2 mL BAC water):

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5 mg/mL = 5,000 mcg/mL. On a 100-unit (1 mL) insulin syringe: 1.6 mg (1,600 mcg) = 32 IU.
Higher dilution option:: Adding 5 mL bacteriostatic water instead gives 2,000 mcg/mL; 1,600 mcg = 80 IU — easier to measure precisely on a small-dose syringe.

Sources:PMID 19467157 PMID 23327199 PMID 39814420 PMID 22010537 PMID 10027483

Substrate the signal needs

Nutritional cofactor precision

Thymosin α1 acts through dendritic cells and Toll-like receptor signaling to steer T-cell responses — it nudges immune output, it does not supply raw fuel. The cofactors here are the nutrients that the immune machinery it targets actually runs on. Reasoned from textbook immune nutrition applied to Tα1's mechanism, not a Tα1 cofactor study.

Reasoned from Tα1's thymic / T-cell mechanism plus established immune nutrition — not a Tα1 cofactor trial. Supplement doses are common evidence-based ranges, not Tα1-specific findings. The honest context holds: real trials exist, the most rigorous was null, and the wellness use is unproven.

Amplify the signal — zinc (the headline cofactor)

Zinc is the single most on-mechanism cofactor for Tα1: thymic hormone output and T-cell maturation are zinc-dependent at a basic biological level.

Mechanism:: Zinc deficiency shrinks the thymus gland and blunts T-cell output — established, textbook immune-nutrition finding. Since Tα1 is itself a thymic peptide that drives dendritic-cell maturation and T-cell polarization, adequate zinc is the substrate the axis it acts on is built from. A deficient zinc status blunts exactly the biology Tα1 is meant to engage.
Protocol integration:: 15–30 mg elemental zinc daily (picolinate or bisglycinate forms); pair with 1–2 mg copper bisglycinate on any course longer than 4 weeks to prevent copper depletion from high zinc intake. Take with food to reduce nausea.

Amplify the signal — vitamin D and selenium

Two additional immune-axis nutrients, both with well-established roles in T-cell function and both commonly deficient.

Vitamin D:: T-cell activation and differentiation require vitamin D signaling — the vitamin D receptor is expressed on activated T-cells, and deficiency impairs the same Th1-polarized response Tα1 promotes. Dose to sufficiency (blood 25-OH-D ≥ 40 ng/mL); typical corrective doses are 2,000–5,000 IU/day, calibrated by labs.
Selenium 100–200 mcg/day:: Selenium supports normal immune-cell function and selenoprotein-dependent antioxidant defense in immune tissue. Selenomethionine is the preferred form; stay within the 100–200 mcg/day range — selenium has a narrow therapeutic window and the upper tolerable limit is 400 mcg/day.

Supply the substrate — protein and vitamin C

Immune cells and antibodies are built from amino acids; vitamin C is required for normal immune-cell function and is rapidly depleted during immune activation.

Adequate protein:: Chronic under-eating of protein blunts any immune signal regardless of what peptide is involved — T-cells, antibodies, and cytokines are all protein-derived. The practical floor is ≥ 1.2 g/kg body weight/day from complete protein sources.
Vitamin C 500–1,000 mg/day:: Vitamin C accumulates in immune cells at concentrations far above plasma levels and supports phagocyte function, NK-cell activity, and T-cell proliferation. Split dosing (e.g., 500 mg morning + 500 mg evening) improves absorption.

Combinations + timing

Stacking notes + timing windows

Tα1's only evidence-backed combination context is its adjunct role in real trials — layered on top of antivirals in hepatitis B, on top of vaccines as a co-adjuvant. That registered adjunct reality, not a wellness cocktail, is the honest framing for stacking. Two other thymic peptides are cross-referenced as family members, not as proven pairings.

Combinations reasoned from complementary mechanisms or the adjunct contexts in actual trials — not regimens studied head-to-head. Tα1's most rigorous trial (Phase 3 sepsis) was null. Any pairing is doubly unproven for wellness use. Anyone on deliberate immunosuppression (e.g., transplant recipients) should treat Tα1 as contraindicated — boosting immune function can work against anti-rejection therapy.

Tα1 + antiviral therapy (the registered adjunct context)

The one combination Tα1 was actually approved for — added on top of lamivudine or peg-interferon in chronic hepatitis B.

Why it works:: Antivirals suppress viral replication; Tα1 nudges the dendritic-cell and T-cell arm toward a Th1-polarized antiviral response. The idea is that the immune system learns to control the virus better while the antiviral holds viral load down — complementary levers on the same infection, not the same lever twice.
The protocol:: 1.6 mg Tα1 subcutaneously twice weekly, run alongside the antiviral per the prescriber's hepatitis-B regimen, for 6–12 months. This is the dose from the positive meta-analysis (8 trials, n=583). All numbers come from the existing dosing table above.
Outcome:: The combination used in the hepatitis-B trials showed higher HBeAg seroconversion (~45% vs ~15%) and virological response — evidence narrow to this indication and population, not generalizable to healthy-person immune support.

Tα1 + vaccine (co-adjuvant use)

Tα1 was studied as a co-adjuvant given alongside influenza and hepatitis-B vaccines in elderly and immunocompromised people who otherwise mount weak antibody responses.

Why it works:: Tα1 drives dendritic-cell maturation and IL-12 production — the same machinery that makes vaccines work more effectively. Giving it around the time of vaccination amplifies the antigen-presenting response that determines how strong the antibody response will be. This is an immunogenicity endpoint, not a clinical-outcome endpoint.
The protocol:: 900 µg/m² subcutaneously twice weekly for 8 doses, co-administered with the vaccine course. (From the vaccine-adjuvant trial; figures come from the existing dosing table.)
Outcome:: Improved antibody titers in vaccine-hyporesponders in the small trials. This is the most scientifically coherent wellness-adjacent use — but the trials were small, and this is still an immunogenicity measure, not a proven clinical-outcome benefit.

Thymic peptide family — Thymulin (FTS) · Thymogen (Oglufanide)

By community convention, Tα1 is grouped with Thymulin (FTS) and Thymogen (Oglufanide) (thymalin) as the thymic peptide family — all nudge immune signaling from a thymic origin.

Why they are grouped:: Thymulin is a zinc-dependent thymic nonapeptide that promotes T-cell maturation and is active only when bound to zinc — mechanistically complementary to Tα1's dendritic-cell / TLR axis. Thymogen (Thr-Glu dipeptide from thymalin, a thymus extract used in post-Soviet clinical practice) acts on a similar immune-regulation logic. All three are thymus-origin immunomodulators.
The honest caveat:: These are family-resemblance groupings reasoned from a shared thymic origin — not regimens studied head-to-head or in combination. Stacking unproven immunomodulators does not make any of them more proven. Pairing multiple immune-active peptides also raises the concern that combined immune stimulation in the wrong context (existing autoimmunity, deliberate immunosuppression) amplifies risk rather than benefit.
Outcome:: No human trial has tested any Tα1 + thymulin or Tα1 + thymogen combination. Any combination is researcher-convention only.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.32 mL
Doses per vial: 6
Concentration: 5 mg/mL

One vial lasts

Daily: 6 days
Every other day: 12 days
5×/week: 8 days

Large draw (32 units). Double-check the vial size and dose — a mcg/mg mix-up produces values like this.

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

Within its studied uses, thymosin α1 has an unusually clean short-term safety record. Across indications the Zadaxin label reports a drug-related adverse-event (side-effect) rate under 1%, dominated by mild local injection-site discomfort or irritation; rarer reports include erythema (skin redness), transient (temporary) muscle atrophy (muscle shrinkage), polyarthralgia with hand edema (aching in multiple joints with hand swelling), and rash. The large double-blind sepsis trial (n=1,089) showed no major safety signal, and the earlier sepsis RCT (randomized controlled trial) reported no serious drug-related adverse events.

There is one clear contraindication to flag: deliberately immunosuppressed patients (such as transplant recipients) — because boosting immune function could undermine anti-rejection therapy — along with known hypersensitivity to the peptide or any component.

The honest limitation is duration and population. The reassuring safety data come from time-limited trials (weeks to about twelve months) in defined patient groups. Robust long-term safety data for the off-label 'wellness,' chronic immune-boosting, or anti-aging use pattern — repeated dosing in healthy people over years — does not exist, and there is no impurity/contamination profile for research-chemical material sold online. This page presents the available trial literature only and makes no therapeutic claim.

Sources:PMID 39814420 FDA human-drug-compounding guidance

As reported in literature

Research dosing ranges

This is the research-evidence table — the doses exactly as they were studied in human clinical trials or stated on the Zadaxin label, shown separately so the trial data is never mistaken for a personal recommendation (this page makes no therapeutic or how-to claim). Unusually for a catalog peptide, these are real human trial doses, not animal extrapolations. Thymosin α1 is given subcutaneously (under the skin); the Zadaxin label states it must NOT be given intravenously (into a vein), and it is supplied as a lyophilized (freeze-dried) powder reconstituted before use. Read the rows together: they span indications with very different results, and the largest, most rigorous trial (sepsis) was negative.

Dose	Route	Model	Outcome	Sources:
1.6 mg, 2×/week, 6–12 months	Subcutaneous	Human — chronic hepatitis B (add-on to lamivudine or peg-interferon); meta-analysis, 8 trials, n=583	Higher HBeAg seroconversion (≈45% vs 15%) and virological response — but small, mostly single-center Chinese add-on trials (moderate-certainty)	PMID 19467157
1.6 mg, 2×/day ×5 days then 1×/day ×2 days	Subcutaneous	Human — severe sepsis RCT (n=361, single-blind, China; ETASS)	28-day mortality 26% vs 35%; log-rank p=0.049 (marginal) — NOT confirmed by the later rigorous trial	PMID 23327199
Every 12 hours ×7 days	Subcutaneous	Human — sepsis Phase 3 RCT (n=1,089, double-blind, placebo-controlled, China; TESTS)	NO mortality benefit: 23.4% vs 24.1%, HR 0.99 (95% CI 0.77–1.27), p=0.93 — the most rigorous trial was NULL	PMID 39814420
Variable (as administered)	Subcutaneous	Human — COVID-19 multicenter retrospective (19 hospitals, n=771)	Apparent mortality benefit DISAPPEARED after propensity matching (51.0% vs 52.9%, not significant) — confounded by indication	PMID 33208294
1.6–6.4 mg + dacarbazine ± interferon-α	Subcutaneous	Human — metastatic melanoma RCT (n=488)	Median OS 9.4 vs 6.6 months, HR 0.80 (95% CI 0.63–1.02), p=0.08 — did NOT reach significance (hypothesis-generating)	PMID 20194853
900 µg/m², 2×/week ×8 doses	Subcutaneous	Human — elderly / immunocompromised, as vaccine co-adjuvant (influenza, hepatitis B)	Improved antibody titers in vaccine-hyporesponders — an immunogenicity endpoint, not a clinical-outcome endpoint; trials small	PMID 22010537

Quick answers

Frequently asked

What is Thymosin Alpha-1?

It is a 28-amino-acid immune-signaling peptide, the N-terminal fragment of a protein called prothymosin alpha, first isolated from thymus extract in 1977. The synthetic version is thymalfasin, sold abroad as the drug Zadaxin. It is an immunomodulator — it adjusts immune signaling, working mainly through dendritic cells.

Does it 'boost the immune system' in healthy people or slow aging?

There is no good trial supporting that. Every meaningful study was done in sick or vulnerable populations (hepatitis B, sepsis, cancer, vaccine non-responders), not in healthy people, and there are zero positive trials for any general 'immune-boosting,' anti-aging, or longevity endpoint. That popular online use is not backed by the evidence.

Does it work for sepsis?

The most rigorous evidence says no. A 1,089-patient double-blind, placebo-controlled Phase 3 trial published in 2025 found no reduction in 28-day mortality (hazard ratio 0.99). That overturned a smaller, single-blind earlier trial that had looked marginally positive — a good example of an effect disappearing when the study design tightens.

What about COVID-19 or cancer?

For COVID-19, the data are observational: an apparent survival benefit in early multicenter records vanished after researchers statistically adjusted for which patients received it. For cancer, the strongest study — a 488-patient melanoma trial — showed a survival trend that missed statistical significance (p=0.08). Neither supports a confident claim of benefit.

Where is the evidence actually supportive?

In two narrow places: as an add-on to chronic hepatitis B therapy (several positive but small, mostly single-center trials and meta-analyses), and for improving vaccine antibody responses in elderly or immunocompromised people. The hepatitis B use is the basis for its approval abroad as Zadaxin.

Is it FDA-approved, and what is its half-life?

It is not FDA-approved in the US and not centrally approved by Europe's EMA, though it is nationally registered as Zadaxin in around 35 countries for chronic hepatitis B. In the US its compounding status is in limbo: the FDA placed it on a 503A safety-risk list in 2023, then removed it in 2024 only because the nomination was withdrawn — not because it was endorsed. Its human half-life after subcutaneous injection is short — under 3 hours in the primary study, commonly cited around 2 hours — and it is given subcutaneously (the label says not intravenously).

Primary sources

References

PubChem CID 16130571PubChem CID 16130571 (Thymalfasin / Thymosin α1; C129H215N33O55, MW 3108.3 avg, monoisotopic 3106.50; 28-aa N-acetylated sequence Ac-SDAAVDTSSEITTKDLKEKKEVVEEAEN; CAS 62304-98-7 / 69521-94-4; FDA UNII W0B22ISQ1C)
PMID 265536Low, Thurman, Goldstein et al., PNAS 1977;74(2):725–729 (isolation + sequence of thymosin α1, an immunologically active thymic polypeptide)
PMID 14982877Romani, Bistoni, Puccetti et al., Blood 2004;103(11):4232–4239 (Tα1 activates dendritic cells for antifungal Th1 resistance through Toll-like receptor signaling — in vitro / mouse)
PMID 19467157Meta-analysis of thymosin α1 + lamivudine vs lamivudine in chronic hepatitis B, 8 trials, n=583 (HBeAg seroconversion 45.1% vs 15.2%; virological response 84.7% vs 74.9%)
PMID 23327199Wu, Li, Liu et al., Crit Care 2013 — ETASS: thymosin α1 in severe sepsis, multicenter single-blind RCT, n=361 (28-day mortality 26.0% vs 35.0%; log-rank p=0.049, marginal); NCT00711620
PMID 39814420TESTS: thymosin α1 for sepsis, multicentre double-blind placebo-controlled Phase 3 RCT, 22 centers, n=1,089 (28-day mortality 23.4% vs 24.1%; HR 0.99, 95% CI 0.77–1.27, p=0.93 — NO benefit)
PMID 33208294Multicenter retrospective COVID-19 study, 19 hospitals, n=771 (unadjusted mortality 41.3% vs 60.6%, but after propensity matching 51.0% vs 52.9%, NOT significant — no association with reduced mortality)
PMID 20194853Maio et al., J Clin Oncol 2010;28(10) — thymosin α1 + dacarbazine ± IFN in metastatic melanoma, RCT n=488 (median OS 9.4 vs 6.6 mo, HR 0.80, 95% CI 0.63–1.02, p=0.08 — missed significance)
PMID 22010537Review: utility of thymosin α1 as co-adjuvant in influenza vaccines / vaccine-hyporesponsive populations (immunogenicity endpoints; e.g. NCT01031966)
PMID 10027483Pharmacokinetics of thymosin α1 after subcutaneous injection in healthy volunteers (rapid absorption, serum half-life ~2 h, no accumulation; well absorbed SC)
FDA human-drug-compounding guidanceFDA — thymosin α1 placed on Category 2 interim 503A bulk drug substances list (Sept 2023; 'may present significant safety risks'), then removed effective 2024-09-27 on withdrawal of the nomination (NOT an affirmative finding; also not on Category 1)

Research use only · Not medical advice · Updated 2026-06-01