Thymosin Alpha-1 — Research Overview
Chemical Name: 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-OH INN (International Nonproprietary Name): Thymalfasin Also Known As: Thymosin Alpha-1, Tα1, TA-1, thymosin fraction 5 alpha-1 component Brand Name: Zadaxin (SciClone Pharmaceuticals / HLB Therapeutics) Molecular Weight: 3,108 Da Structure: Synthetic 28-amino acid acetylated polypeptide. N-terminally acetylated (Ac-Ser) — this N-terminal acetylation is a defining structural feature that is identical to the naturally occurring human peptide produced by thymic stromal cells. The acetylation protects the N-terminus from aminopeptidase degradation and is essential for full biological activity. Relationship to Thymosin Beta-4 / TB-500: Thymosin Alpha-1 and Thymosin Beta-4 (TB-500) share only the word “thymosin” and their historical origin in thymic tissue extracts. They are pharmacologically independent compounds with different amino acid sequences, different molecular mechanisms, different receptor targets, and different clinical applications. Tα1 is a 28-aa immune regulatory peptide acting through toll-like receptors and T-cell maturation pathways. TB-500 is a fragment of the 43-aa actin-sequestering protein Tβ4, acting through cytoskeletal dynamics. They are often confused but should not be conflated. Discovery: Thymosin was first isolated from calf thymus tissue by Allan Goldstein and colleagues at the National Cancer Institute in 1966 as a lymphocyte production factor. Thymosin fraction 5 (TF5) — a complex mixture of small peptides — was the initial purified extract. Thymosin Alpha-1 was purified and separated from TF5 in 1977 and found to possess 10-1,000 times higher biological activity than the unfractionated TF5. Synthetic thymalfasin — chemically identical to native human Tα1 — was subsequently developed to enable consistent pharmaceutical production. International Regulatory Status: Approved for clinical use in more than 35 countries under the Zadaxin brand name, primarily for chronic hepatitis B, hepatitis C (in combination with interferon), and as an immune adjuvant in oncology settings. Approved markets include China (major market), Italy, South Korea, India, the Philippines, Singapore, multiple Latin American countries, the Middle East, and Southeast Asia. United States Regulatory Status: Not FDA-approved for any therapeutic indication. FDA orphan drug designations granted for: chronic active hepatitis B, malignant melanoma, DiGeorge anomaly with immune defects, and hepatocellular carcinoma. Orphan drug designation is a regulatory incentive program — it is not drug approval and does not authorize marketing or use. In 2023, the FDA placed thymosin alpha-1 on the Category 2 bulk drug substance list, restricting compounding pharmacy access under 503A regulations, citing concerns about peptide purity characterization and immunogenicity risk from certain routes of administration. In February 2026, HHS Secretary Kennedy announced that thymosin alpha-1 is among peptides expected to return to Category 1 status, which would restore legal compounding access under physician prescription. This regulatory evolution is ongoing and researchers should verify current status at time of use. European Regulatory Status: Not EMA-centrally approved. Orphan designation granted by EMA Committee for Orphan Medicinal Products (EU/3/02/110) for hepatocellular carcinoma. Pharmacokinetics: Thymalfasin is rapidly absorbed after subcutaneous injection. Peak serum concentrations are achieved within approximately 2 hours. Serum half-life is approximately 2 hours. Blood levels return to baseline within 24 hours. Despite the short half-life, biological effects are sustained — consistent with receptor-mediated immune programming rather than continuous receptor occupancy requirement. WADA Status: Not specifically listed on the WADA prohibited list as of this compilation. Category: Endogenous thymic immunomodulatory peptide / TLR2/TLR9 agonist / T-cell maturation promoter / dendritic cell activator / NK cell enhancer / internationally approved pharmaceutical / FDA orphan drug designation holder / research tool for immunology and innate/adaptive immune interface
Research Use Only — Disclaimer
The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption outside of any applicable prescription pharmaceutical context. The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.
What Is Thymosin Alpha-1?
Thymosin Alpha-1 is a 28-amino acid endogenous peptide produced by thymic stromal cells that plays a central role in the development, maturation, and functional calibration of T lymphocytes — the adaptive immune system’s primary cellular effectors. It belongs to the alpha-thymosin family of peptides that regulate the thymus gland’s function as the organ where T-cells develop the capacity to distinguish self from non-self, and where the adaptive immune system’s defensive repertoire is established and maintained.
The thymus is most active during fetal development and early childhood, producing the highest concentrations of Tα1 during this period. With age, the thymus undergoes progressive involution — structural atrophy beginning in early adulthood and accelerating throughout life — with accompanying decline in thymic hormone production including Tα1. This thymic involution is considered one of the primary mechanisms underlying immunosenescence: the progressive deterioration of immune function that leaves older adults increasingly vulnerable to infection, malignancy, and vaccine non-responsiveness. The decline in Tα1 production with age has made it a subject of particular interest in geroscience and longevity medicine as a potential tool for restoring immune competence.
Thymosin Alpha-1’s most important pharmacological property is that it is an immune modulator rather than a simple immune stimulant. This distinction is mechanistically essential. A pure immune stimulant raises all immune activity indiscriminately — potentially worsening inflammatory conditions, autoimmune responses, and cytokine-driven pathology. An immune modulator calibrates the immune system toward appropriate responses: upregulating deficient immunity (as in chronic viral infection, cancer-associated immunosuppression, or post-chemotherapy lymphopenia) while also having anti-inflammatory properties that prevent immune overactivation (as in cytokine storm or sepsis-associated immune dysfunction). This bidirectional calibrating property — immunostimulatory where needed, immunoregulatory where overactivation occurs — is the defining clinical advantage that has driven Tα1’s use across such a broad spectrum of conditions where immune calibration is the therapeutic goal.
The Thymus — Biology and Tα1’s Physiological Context
The thymus is a bilobed lymphoid organ located in the anterior mediastinum, directly behind the sternum. Its primary function is the education and selection of T lymphocytes from bone marrow-derived precursor cells. T-cell progenitors migrate to the thymus and undergo a two-stage selection process: positive selection (retaining only T cells whose T-cell receptors can recognize self-MHC molecules) and negative selection (eliminating T cells that react too strongly to self-antigens, preventing autoimmunity). This education process produces the functionally competent, self-tolerant T lymphocytes that circulate throughout the body as the adaptive immune system’s cellular defense force.
Thymic stromal cells — epithelial cells, dendritic cells, and macrophages within the thymic microenvironment — produce multiple thymic hormones including Tα1, thymosin beta-4, thymopoietin, and thymulin. These hormones coordinate the T-cell maturation process and regulate the thymic microenvironment. Tα1 specifically promotes the differentiation of immature thymocytes (precursor T cells) into mature, functionally competent T lymphocytes, and maintains the biological activity of mature T cells in the periphery.
With advancing age, thymic involution dramatically reduces the organ’s T-cell production capacity and its hormonal output. This is accompanied by a progressive shift in the peripheral T-cell pool from naive T cells (capable of responding to new antigens) to memory T cells (specialized for previously encountered antigens but incapable of mounting effective responses to novel pathogens or cancer neoantigens). This immunological narrowing directly contributes to the increased susceptibility to new infections, reduced vaccine responses, and increased cancer risk associated with aging. Exogenous Tα1 supplementation is proposed to partially compensate for this thymic decline by providing the hormonal signal that the aging thymus no longer produces in adequate quantities.
Mechanism of Action
Toll-like receptor activation — innate immunity gating: Tα1’s primary molecular mechanism involves activation of toll-like receptors (TLRs), particularly TLR2, TLR3, TLR4, TLR7, and TLR9. TLRs are pattern recognition receptors on innate immune cells that detect pathogen-associated molecular patterns (PAMPs) — the molecular signatures that distinguish microbial and viral threat from self. By activating TLRs — particularly in myeloid dendritic cells (via TLR2/TLR4) and plasmacytoid dendritic cells (via TLR9) — Tα1 triggers downstream signaling through IRF3 and NF-kB pathways, leading to interferon-gamma (IFN-γ), interleukin-2 (IL-2), and other cytokine production. This TLR-mediated innate immune activation is the upstream signal that subsequently drives the adaptive T-cell responses for which Tα1 is best known.
T-cell maturation and differentiation: Tα1 directly promotes the maturation of immature T-cell precursors (pro-T cells and pre-T cells) into functionally competent CD4+ helper T cells and CD8+ cytotoxic T cells. It downregulates the activity of terminal deoxynucleotidyl transferase (TdT) in TdT-positive thymocytes — a marker of immature thymocytes — facilitating their transition to mature T-cell phenotypes. This direct thymocyte maturation activity supports the expansion of the naive T-cell pool and restores immune competence in states of T-cell lymphopenia, whether caused by aging, HIV infection, chemotherapy, or other immunosuppressive conditions.
T-cell exhaustion reversal: One of the most clinically significant recently characterized mechanisms of Tα1 is its ability to reverse T-cell exhaustion — the dysfunctional state of T cells that have been chronically exposed to antigen (as in persistent viral infection or cancer) and have downregulated their effector functions. Exhausted T cells are characterized by expression of inhibitory receptors (PD-1, LAG-3, TIM-3) and impaired cytokine production. In COVID-19 studies, Tα1 was shown to restore lymphocyte counts and reverse T-cell exhaustion signatures in severe cases — a mechanism directly relevant to the immune paralysis that characterizes severe viral infections and cancer-associated immunosuppression.
Dendritic cell activation and maturation: Tα1 promotes the maturation, differentiation, and antigen-presenting function of dendritic cells — the immune system’s primary professional antigen-presenting cells that bridge innate detection of pathogens to adaptive T-cell activation. Enhanced dendritic cell function explains Tα1’s vaccine-adjuvant properties: by priming dendritic cells to more effectively present vaccine antigens to T cells, Tα1 enhances both the magnitude and durability of vaccine-induced immune responses.
NK cell activation: Tα1 activates natural killer (NK) cells — the innate immune system’s primary non-MHC-restricted cytotoxic effectors that kill virally infected cells and cancer cells. Enhanced NK cell activity contributes to both the antiviral and antitumor effects observed in Tα1 clinical studies.
MHC class I upregulation: Tα1 increases expression of major histocompatibility complex class I (MHC-I) molecules on antigen-presenting cells and tumor cells. MHC-I presentation of viral or tumor antigens is required for CD8+ cytotoxic T cell recognition and killing. This mechanism directly enables immune clearance of virally infected cells and cancer cells that have downregulated MHC-I (a common immune-evasion strategy in both chronic viral infection and oncology contexts).
Anti-inflammatory modulation: Despite its role in immune activation, Tα1 also suppresses excessive inflammatory signaling — particularly IL-1β and TNF-α production. This anti-inflammatory dimension is mechanistically explained by Tα1’s promotion of regulatory T-cell (Treg) activity and macrophage M1-to-M2 phenotypic transition, shifting the inflammatory environment toward tissue repair rather than continued inflammation. This dual immune-activating and anti-inflammatory profile explains the apparently paradoxical efficacy of Tα1 in both immunodeficiency states (where immune activation is needed) and inflammatory states (where immune modulation is needed).
Published Research
Study 1 — First Controlled Clinical Trial: Hepatitis B Viral Clearance
Authors: Mutchnick MG, et al. Year: 1991 (pilot); 1999 (pivotal Phase 3) Journal: Multiple publications, primarily Gastroenterology and Hepatology
The foundational human clinical evidence for Tα1 was established in a series of hepatitis B trials spanning 1991 to the late 1990s. In the 1991 pilot trial in 12 chronic HBV patients, the Tα1-treated group showed 86% HBV DNA clearance versus 20% for placebo (P less than 0.04), with improvements in aminotransferases, lymphocyte counts, and IFN-γ production persisting through 26 months of follow-up. This early dramatic result drove the subsequent development program.
The pivotal Chien et al. (1998) randomized controlled trial compared 26-week treatment, 52-week treatment, and untreated observation. At 18-month follow-up, complete virological response rates were 40.6% (26-week course, P equal to 0.004), 26.5% (52-week course), and 9.4% (untreated controls). The 26-week course’s superiority established the standard treatment duration used in subsequent international trials.
Mutchnick et al. (1999) conducted the pivotal Phase 3 multicenter, double-blind, placebo-controlled trial in 97 HBeAg-positive patients, which together with the earlier efficacy data supported the FDA’s orphan drug designation decisions and served as the registration basis for international approvals.
The hepatitis B evidence base now encompasses multiple RCTs and meta-analyses across hundreds of patients, making hepatitis B the most thoroughly characterized indication for Tα1. An important context note: the clinical landscape for hepatitis B has been transformed by direct-acting antivirals since these trials were conducted. In the current standard-of-care era, nucleoside analogs (tenofovir, entecavir) achieve highly effective viral suppression with simpler dosing regimens, repositioning Tα1 from a primary antiviral agent to a potential adjunct immunomodulatory therapy in patients with incomplete immune reconstitution on antiviral therapy.
Study 2 — Hepatitis C Combination Therapy
Authors: Multiple investigators; Sherman (meta-analysis), multiple Phase 2/3 trials Year: 1996-2004
Multiple clinical trials evaluated Tα1 in hepatitis C, primarily as combination therapy with interferon-alpha. The most clinically significant finding was that Tα1 plus IFN-alpha produced substantially higher viral clearance and ALT normalization rates than IFN-alpha monotherapy. In one trial, combination therapy achieved normal serum ALT at six months in 71% of patients versus 35% with IFN-alpha alone. HCV RNA clearance occurred in 65% of combination-treated patients versus 29% with IFN-alpha alone. A meta-analysis by Sherman confirmed the superiority of combination therapy over interferon monotherapy across available trials.
The same contextual note applies as in hepatitis B: HCV treatment has been revolutionized by direct-acting antivirals since these trials were conducted, with current HCV regimens achieving 95%+ cure rates regardless of immune status. The hepatitis C indication for Tα1 is now primarily of historical research significance.
Study 3 — Cancer Immunotherapy Adjunct
Authors: Multiple investigators; various Phase 2 trials in hepatocellular carcinoma, NSCLC, melanoma, and other cancers
An extensive body of Phase 2 clinical trials has evaluated Tα1 as an adjunct to chemotherapy and other cancer treatments. The consistent finding across tumor types is that Tα1 does not directly kill cancer cells but preserves and restores the immune system’s anti-tumor capacity during immunosuppressive cancer treatment.
In hepatocellular carcinoma (HCC), Tα1 combined with transarterial chemoembolization (TACE) demonstrated improved survival compared to TACE alone in a randomized controlled trial — providing the basis for ongoing large-scale multicenter trials in China investigating Tα1’s effect on 2-year recurrence-free survival after curative HCC resection (NCT02281266, enrolling patients receiving thymalfasin 1.6 mg twice weekly for 12 months).
In non-small cell lung cancer, a Phase 2 controlled trial of Tα1 plus low-dose IFN-alpha after ifosfamide showed improved clinical outcomes compared to chemotherapy alone. Similar adjunctive benefits were documented in melanoma trials.
The antitumor mechanism operates through multiple pathways: restoring chemotherapy-suppressed T-cell counts and function, activating NK cells against tumor targets, upregulating MHC-I on tumor cells to enable CD8+ cytotoxic recognition, enhancing dendritic cell antigen presentation, and reversing tumor-induced T-cell exhaustion. These mechanisms position Tα1 as a rational complement to immunotherapy approaches (checkpoint inhibitors, cancer vaccines) that also depend on functional T-cell immunity.
Study 4 — Sepsis and Immunosuppression in Critical Illness
Authors: Multiple; Wu J et al. (major Chinese RCT); TESTS trial
Sepsis and septic shock cause a paradoxical immune response: an initial hyperinflammatory phase followed by profound immunosuppression (immunoparalysis) characterized by lymphopenia, T-cell exhaustion, and impaired innate immune function. This sepsis-induced immunosuppression — not the initial cytokine storm — is what kills most sepsis patients through secondary infections and organ failure. Tα1’s immune-restoring properties make it mechanistically rational for this phase of sepsis.
Multiple Chinese randomized trials demonstrated significant reductions in mortality associated with Tα1 treatment in sepsis and septic shock patients, with consistent findings of reduced 28-day mortality, restored lymphocyte counts, and reduced secondary infections. A systematic review and meta-analysis of these trials showed statistically significant mortality benefit in the Tα1-treated groups.
The TESTS trial — the largest sepsis trial conducted to date for Tα1, with 1,106 patients across multiple centers — did not meet its primary endpoint of 28-day mortality reduction. This important negative result from a rigorous, adequately powered trial introduced meaningful uncertainty into the sepsis indication and is the largest single qualification to the sepsis evidence base. The discordance between the positive smaller trials and the negative TESTS result is consistent with known publication bias and effect size inflation in smaller trials and should be acknowledged honestly. The sepsis application of Tα1 remains under active investigation but cannot be considered established.
Study 5 — COVID-19: T-Cell Exhaustion Reversal
Authors: Liu Y et al. and multiple other COVID-19 investigators Year: 2021-2023
The intersection of Tα1’s T-cell exhaustion reversal mechanism with the specific immune dysregulation of severe COVID-19 generated substantial clinical interest during the pandemic. COVID-19-associated lymphopenia — primarily affecting CD4+ and CD8+ T cells — and the T-cell exhaustion phenotype (elevated PD-1, TIM-3, LAG-3 on circulating T cells) characterized severe disease and correlated with poor outcomes.
Liu et al. retrospectively reviewed 76 severe COVID-19 cases from Wuhan and found that Tα1 treatment was associated with restoration of lymphocyte counts, reduction in T-cell exhaustion markers, and reduced mortality in severe cases — establishing proof-of-concept for Tα1’s mechanistic relevance to COVID-19 immune pathology.
Multiple subsequent studies evaluated Tα1 in COVID-19, with generally positive results in terms of lymphocyte restoration, immune biomarker normalization, and clinical outcomes. However, conflicting findings emerged — notably one study finding no beneficial effect on CD4+ and CD8+ T-cell restoration — highlighting that the COVID-19 immune response is heterogeneous and that Tα1’s benefit likely varies by disease phase, severity, and immune baseline.
Tα1 was also studied as a vaccine adjuvant for COVID-19 vaccination in elderly and immunocompromised populations, where standard vaccine immune responses are frequently suboptimal. Its mechanism of enhancing dendritic cell function and T-cell priming provides biological rationale for this application.
Study 6 — Vaccine Enhancement in Immunocompromised Populations
Authors: Multiple; hemodialysis patients, elderly populations, HIV
Tα1’s ability to enhance vaccine immunogenicity in populations with compromised immune function is one of its most consistently demonstrated properties and one where the clinical logic is straightforward: patients who respond poorly to standard vaccination have insufficient T-cell and dendritic cell function to generate protective immune memory; Tα1 restores these functions.
A pilot study demonstrated that Tα1 enhanced immunogenicity of an adjuvanted pandemic H1N1 influenza vaccine (Focetria) in hemodialyzed patients — a population known for poor vaccine responses due to uremia-induced immune dysfunction.
Multiple studies in elderly populations — who are similarly immunocompromised relative to young adults — showed improved antibody titers and T-cell responses to influenza vaccination when Tα1 was administered as an adjunct. This vaccine-enhancement application is currently under Phase 3 trial investigation (NCT06821100) evaluating Tα1 as an enhancer of vaccine response among older adults.
The US Regulatory Story — An Honest Account
Tα1’s US regulatory history is complex and requires accurate characterization rather than simplified claims in either direction. The key facts are:
Thymalfasin (Zadaxin) received FDA orphan drug designations for chronic active hepatitis B, malignant melanoma, DiGeorge anomaly, and hepatocellular carcinoma. Orphan drug designation is a regulatory incentive (7-year market exclusivity, fee waivers, expedited review access) granted when a drug shows potential for treating a rare disease. It is explicitly not approval, and the FDA’s orphan drug database lists thymalfasin as “Not FDA Approved for Orphan Indication” for these designations.
SciClone Pharmaceuticals conducted clinical development primarily in Asian markets where hepatitis B prevalence, regulatory environment, and commercial viability favored development. The commercial decision not to pursue the full FDA approval pathway in the United States — which would require US-conducted Phase 3 trials meeting FDA-specific endpoints — left Tα1 without an approval pathway despite its international approval status.
In 2023, the FDA placed Tα1 on the Category 2 restricted bulk drug substance list, which restricted compounding pharmacies from preparing it under 503A rules. The FDA’s reasoning cited concerns about peptide purity characterization complexity and immunogenicity risk from certain routes of administration — quality and manufacturing concerns rather than efficacy concerns.
In February 2026, HHS Secretary Kennedy announced an expectation that Tα1 and approximately 14 other peptides would be restored to Category 1 status, which would again permit licensed compounding pharmacies to prepare it under physician prescription. As of this compilation, this regulatory change is anticipated but should be verified for current status.
The broader analytical conclusion from this regulatory trajectory: Tα1 has more validated human clinical evidence than the vast majority of research peptides available in Western markets, backed by international approvals in 35+ countries. Its US regulatory absence reflects commercial strategy, regulatory process incompatibilities between clinical practice settings (where the most rigorous Tα1 evidence was generated) and FDA trial design requirements, and manufacturing quality concerns specific to peptide compounding — not a finding of inefficacy or safety concern.
Tα1 vs Thymosin Beta-4 / TB-500 — Clear Disambiguation
Because both compounds use the word “thymosin” and both originate from historical thymic tissue research, they are frequently confused. The distinction is absolute and pharmacologically important.
Thymosin Alpha-1 (Tα1) is a 28-aa immune regulatory peptide. Its target is the immune system — specifically T-cell development, dendritic cell activation, NK cell function, and TLR-mediated innate immunity. It has no direct effects on actin, cell migration for tissue repair, angiogenesis, or connective tissue regeneration.
Thymosin Beta-4 (Tβ4, TB-500) is a 43-aa (or 7-aa active fragment) actin-sequestering peptide. Its target is the cytoskeleton and tissue repair biology — actin dynamics, cell migration to wound sites, angiogenesis via VEGF, and ILK-mediated cardiac repair. It has no direct T-cell maturation, TLR activation, or adaptive immune modulating effects comparable to Tα1.
The shared “thymosin” nomenclature is a historical artifact of both being discovered in thymic tissue extracts before their mechanisms were understood. They are as pharmacologically different as any two compounds in this catalog.
Safety Profile
Tα1/thymalfasin has one of the best-characterized safety profiles of any compound in this catalog, with data from over 11,000 clinical trial participants across multiple disease conditions and decades of post-marketing use in 35+ countries.
The dominant finding across all clinical experience is that Tα1 is well-tolerated with an adverse event profile essentially indistinguishable from placebo injection in most trials. Local injection site reactions (mild redness, swelling, pain) are the most commonly reported events. No clinically significant systemic adverse effects, organ toxicity, drug interactions, or serious adverse event patterns have been identified in the published clinical literature.
The FDA’s 2023 concerns about immunogenicity risk and peptide purity characterization are manufacturing and quality control concerns rather than inherent safety concerns about the Tα1 molecule itself. These concerns apply to the compounding context where quality control variability between pharmacies is a genuine regulatory issue — not to the well-characterized pharmaceutical-grade Zadaxin formulation used in international clinical trials.
Thymalfasin is not associated with autoimmune exacerbation despite its immune-activating properties — the immunomodulatory rather than immunostimulatory nature of its mechanism means it calibrates toward appropriate immune responses rather than indiscriminate activation.
Current Research Status and Active Investigations
Tα1 remains an active area of investigation across multiple fronts. The large-scale multicenter Chinese RCT evaluating Tα1 as an adjunct after curative HCC resection (NCT02281266) continues to accrue patients. Phase 3 vaccine enhancement trials in elderly adults are ongoing. Research into post-COVID immune restoration and long COVID immune dysregulation is emerging. Investigation of Tα1 in combination with checkpoint inhibitor cancer immunotherapy — where its T-cell exhaustion reversal mechanism is highly relevant to the primary resistance mechanisms of checkpoint inhibitor therapy — is generating preclinical and early clinical data.
The US regulatory trajectory following the anticipated 2026 Category 1 restoration will determine whether American research and clinical communities can access thymalfasin more readily through compounding pharmacy channels.
Reconstitution Note
Thymosin Alpha-1 is supplied as lyophilized powder. Bacteriostatic water is the standard reconstitution solvent for research use. The pharmaceutical Zadaxin formulation is supplied as a lyophilized powder containing 1.6 mg thymalfasin, 50 mg mannitol, and sodium phosphate buffer at pH 6.8, reconstituted with 1 mL sterile water for injection. For research applications, always confirm the recommended solvent against the specific lot datasheet before reconstitution.
In-Use Period and Storage
Before Reconstitution — Lyophilized Powder
Rogue Compounds stores all products refrigerated prior to shipping to maintain compound integrity from production through to delivery. Upon receipt researchers should store vials at 2 to 8 degrees Celsius immediately. Keep vials sealed, dry, and away from direct light until ready for use. Do not freeze. Repeated freeze-thaw cycling has been documented in peer-reviewed pharmaceutical formulation literature to accelerate structural degradation even in dry powder form, potentially compromising molecular integrity and experimental reproducibility.
Why We Refrigerate Instead of Freeze
Freezing and thawing introduces mechanical and osmotic stress at the molecular level. Published pharmaceutical research identifies freeze-thaw cycling as a significant risk factor for loss of structural integrity in peptides and protein-based compounds. To protect compound quality at every stage of handling and fulfillment, Rogue Compounds maintains refrigerated rather than frozen cold chain storage throughout the entire process.
After Reconstitution — Liquid Solution
Store reconstituted solutions refrigerated at 2 to 8 degrees Celsius immediately after preparation. Use within the timeframe recommended for the individual compound. Label each aliquot with the compound name, concentration, date of reconstitution, and diluent used. Discard any solution that shows visible particulate matter, discoloration, or signs of degradation.
Note: Storage and in-use recommendations on this page are provided as general laboratory guidance based on standard peptide handling practices documented in peer-reviewed pharmaceutical literature. Researchers should always refer to the individual compound’s published research literature and datasheet for any specific requirements. All products sold by Rogue Compounds are intended strictly for in-vitro laboratory research use only.
Available from Rogue Compounds
View the Thymosin Alpha-1 product page: https://roguecompounds.com/product/thymosin-alpha-1/