Thymosin Beta-4 [Nasal Spray]

Description

What is TB-500 Nasal Spray?

TB-500  is a synthetic N-terminal-acetylated heptapeptide corresponding to residues 17-23 of thymosin beta-4 (Tβ4), a 43-amino acid endogenous polypeptide expressed in virtually all nucleated mammalian cells. The seven-amino acid sequence Leu-Lys-Lys-Thr-Glu-Thr-Gln (LKKTETQ) represents the actin-binding domain of the parent Tβ4 protein, the region identified as responsible for G-actin sequestration, a function critical for regulating actin polymerization dynamics, cytoskeletal remodeling, and cell migration. The N-terminal acetyl group (Ac-) is a synthetic modification applied at the leucine residue that provides resistance to aminopeptidase-mediated degradation relative to the non-acetylated form, while preserving the actin-binding function of the LKKTETQ sequence.

TB-500 is chemically, structurally, and pharmacologically distinct from full-length thymosin beta-4 (Tβ4; CAS 77591-33-4; MW approximately 4963 g/mol; CID 16132341). Full-length Tβ4 is a 43-amino acid protein with a broader biological activity profile encompassing the LKKTETQ actin-binding domain at residues 17-23 plus additional structural and functional domains not present in TB-500. Published human clinical trial data – including the RGN-259 topical ophthalmic program for corneal wound healing and the venous ulcer program – was generated using full-length Tβ4, not the TB-500 heptapeptide fragment. The two molecules have different chemical identities, different molecular weights, different CAS numbers, and different regulatory histories. Clinical and preclinical data for full-length Tβ4 cannot be directly applied to the TB-500 fragment.

Neither TB-500 nor full-length Tβ4 has been approved by the Food and Drug Administration for any human therapeutic indication. TB-500 was classified as an FDA 503A Category 2 bulk drug substance in late 2023 and subsequently removed from Category 2 effective April 15, 2026. Both TB-500 and full-length Tβ4 are scheduled for Pharmacy Compounding Advisory Committee (PCAC) evaluation at the July 23-24, 2026 hearing under Docket No. FDA-2025-N-6895. Removal from Category 2 does not authorize compounding; TB-500 remains unavailable for legitimate compounding until after the PCAC review and any subsequent FDA rulemaking. The research-grade nasal spray formulation supplied by RCDbio is not a pharmaceutical product and is not equivalent to any compounded or pharmaceutical formulation.

The nasal spray formulation is investigated as a delivery route in preclinical research contexts, based on evidence of olfactory bulb-mediated CNS transport for peptide compounds administered intranasally in rodent models. Intranasal delivery has been studied for its potential to bypass hepatic first-pass metabolism and enhance CNS and systemic bioavailability relative to parenteral routes in preclinical pharmacokinetic models. The nasal mucosa’s proximity to the central nervous system via the olfactory nerve makes it a research-relevant delivery route for CNS-active research compounds.

DISCLAIMER: TB-500 Nasal Spray as supplied by RCDbio is not a dietary supplement and has not been approved by the Food and Drug Administration for human use, veterinary use, consumption, or any therapeutic application. This product is not intended for human consumption or therapeutic self-administration. It is supplied exclusively for in vitro and preclinical laboratory research purposes. All RCDbio research compounds are for laboratory and research purposes only.

Chemical Properties of TB-500

How Does TB-500 Work?

TB-500 does not act through a classical receptor in the conventional pharmacological sense. Its primary documented biological activity is G-actin sequestration,  binding monomeric (globular, G-actin) actin, and regulating the equilibrium between free G-actin and polymerized filamentous actin (F-actin). The LKKTETQ sequence at residues 17-23 of thymosin beta-4 is the region within the parent Tβ4 protein identified as responsible for actin binding and cell migration-promoting activity. Because the Ac-LKKTETQ fragment retains this domain, TB-500 is studied as a tool compound for investigating actin cytoskeletal dynamics, cell migration, wound healing signaling, and actin-dependent vascular processes in preclinical research model systems. The following mechanistic observations are from in vitro and preclinical data only. All observations attributing ILK/Akt signaling to the “Tβ4” class are explicitly derived from full-length 43 AA thymosin beta-4; unless otherwise stated, the extent to which the TB-500 7 AA fragment independently activates ILK/Akt has not been established in published peer-reviewed literature as of June 2026.

G-Actin Sequestration and Actin Polymerization Dynamics

The LKKTETQ actin-binding sequence of Tβ4 sequesters monomeric G-actin in a 1:1 complex, reducing the pool of free G-actin available for polymerization into F-actin filaments. This sequestering activity is the mechanistic basis for Tβ4’s role as the most abundant G-actin buffering protein in mammalian cells. By regulating the available pool of G-actin, the LKKTETQ domain influences the dynamics of actin cytoskeletal remodeling at the leading edge of migrating cells – the lamellipodia and filopodia formation processes that drive cell migration. This G-actin sequestration mechanism is directly relevant to endothelial cell migration, keratinocyte migration at wound edges, and the directed movement of progenitor cells to sites of tissue injury. The synthetic acetylation at the N-terminus of LKKTETQ in TB-500 provides aminopeptidase resistance relative to the non-acetylated form [Esposito et al., 2012; PMID 22962027].

Tβ4 Class Activity: ILK/Akt Pathway Activation and Endothelial Progenitor Cell Survival

The parent compound thymosin beta-4 (full 43 AA form) has been characterized as activating integrin-linked kinase (ILK) in endothelial progenitor cell (EPC) preparations. Full-length Tβ4 causes concentration-dependent increases in EPC viability and proliferation, inhibits apoptosis under serum deprivation, decreases caspase-3 and caspase-9 expression, and markedly increases the Bcl-2/Bax ratio. ILK-Akt activation is required for the anti-apoptotic effect, as demonstrated by ILK-siRNA abolishment; JNK MAPK activation is also involved [Zhao et al., 2011; PMID 21935929]. These observations characterize the full 43 AA Tβ4 protein; the extent to which the TB-500 Ac-LKKTETQ heptapeptide independently recapitulates ILK/Akt anti-apoptotic signaling has not been established in published peer-reviewed literature as of June 2026. Researchers should not assume mechanistic equivalence between full-length Tβ4 and the TB-500 fragment for ILK/Akt pathway studies.

Endothelial Cell Differentiation, Angiogenesis, and Keratinocyte Migration

The thymosin beta-4 class of compounds – acting through the actin-binding domain – has been associated with endothelial cell differentiation, angiogenesis in dermal tissue preparations, keratinocyte migration at wound edges, and collagen deposition in preclinical model systems. TB-500 (Ac-LKKTETQ) is studied in these research contexts as the minimal actin-binding domain fragment responsible for these activities in the parent Tβ4 protein. The compound’s actin sequestration activity at wound-edge cells is proposed to facilitate the leading-edge cytoskeletal dynamics required for directed migration toward wound sites. The N-terminal acetylation protects TB-500 from rapid aminopeptidase degradation in biological fluids, potentially extending the window of actin-binding activity at tissue sites.

Critical Distinction: TB-500 Fragment vs. Full-Length Tβ4

TB-500 (Ac-LKKTETQ; 7 AA; MW 889 g/mol) and full-length Tβ4 (43 AA; MW ~4963 g/mol) are not the same compound. TB-500 retains the actin-binding domain but lacks the additional structural, regulatory, and signaling regions of the parent protein. Published human and animal clinical trial data, including wound healing, corneal repair (RGN-259 ophthalmic program), and venous ulcer studies,  were generated using full-length Tβ4, not the TB-500 fragment. Preclinical biological activity reported for full-length Tβ4 cannot be assumed to apply in equivalent magnitude to the TB-500 fragment. Researchers designing experiments with TB-500 should specify the fragment form in their protocols and cite appropriate fragment-specific or parent-protein data with clear source transparency.

Intranasal Delivery & Pharmacokinetics

Olfactory Bulb-Mediated CNS Transport

When administered intranasally in preclinical rodent model systems, peptide compounds can access the central nervous system through the olfactory nerve (cranial nerve I) pathway. Compounds deposited on the olfactory mucosa are transported along olfactory axons through the cribriform plate to the olfactory bulb, from which access to deeper CNS structures has been characterized in rodent preparations. The olfactory and trigeminal nerve pathways for nose-to-brain peptide transport have been investigated in preclinical studies of peptide and protein delivery [Wong et al., 2024; PMID 38441832]. No compound-specific intranasal CNS delivery data has been published for TB-500 as of June 2026. Peripheral tissue targets for actin-binding activity, wound edges, endothelial cells, keratinocytes, and vascular progenitor cells, are research-relevant targets accessible via systemic absorption following nasal mucosal uptake.

N-Terminal Acetylation and Nasal Mucosal Stability

A relevant structural feature of TB-500 for intranasal research is the N-terminal acetyl group on the leucine residue. The nasal mucosa expresses aminopeptidases that would rapidly degrade the non-acetylated LKKTETQ sequence by cleavage of the free N-terminal amino group. The acetylation blocks this cleavage site, potentially improving the stability of TB-500 at the nasal mucosa relative to non-acetylated actin-binding peptide fragments. This is a structural-chemical observation and does not constitute evidence of intranasal bioavailability or biological activity in any organism.

Nasal Mucosal Absorption

TB-500 (Ac-LKKTETQ) has a molar mass of 889.018 g/mol (~0.89 kDa) – among the smallest molecular weights in the RCDbio nasal spray research range. At this size, nasal mucosal absorption via paracellular and transcellular mechanisms is favorable. The mixed hydrophilic-lipophilic character of the heptapeptide – with two basic lysine residues, hydroxyl-containing threonines, and the hydrophobic N-terminal acetyl-leucine – means nasal absorption will involve both passive paracellular transport and transporter-mediated uptake. Specific nasal mucosal permeability data for Ac-LKKTETQ has not been published.

Compound-Specific Pharmacokinetics

No formal intranasal pharmacokinetic data (plasma half-life, Tmax, Cmax, bioavailability) has been published for TB-500 as of June 2026. TB-500 is susceptible to protease degradation in biological fluids, with the N-terminal acetyl modification providing partial protection. The compound’s small size (~0.89 kDa) and the absence of DPP-IV cleavage sites in its sequence suggest a more favorable nasal mucosal stability profile than larger or DPP-IV-susceptible peptides in this range. Researchers should account for the absence of published intranasal pharmacokinetic data when designing laboratory protocols.

Key Research Findings

Synthesis and Characterization of Ac-LKKTETQ – The N-Terminal Acetylated 17-23 Fragment of Thymosin Beta-4 Identified in TB-500 (HPLC/HRMS, Human Tβ4 Sequence, In Vitro Characterization): First scientific characterization of TB-500 as a distinct compound containing the Ac-LKKTETQ sequence; identification by high-performance liquid chromatography and high-resolution mass spectrometry using Orbitrap technology; Ac-LKKTETQ confirmed as the N-terminal acetylated 17-23 fragment of human thymosin beta-4; synthetic Ac-LKKTETQ prepared by solid-phase peptide synthesis and analytical detection strategy developed for plasma and urine [Esposito et al., 2012; PMID 22962027]

Thymosin Beta-4 (Full 43 AA Form) Activates ILK/Akt and Inhibits Endothelial Progenitor Cell Apoptosis (Human EPC Cell Preparation – Class-Level Evidence for Tβ4; Not TB-500 Fragment): Full-length Tβ4 caused concentration-dependent increases in EPC viability and proliferation, inhibited apoptosis under serum deprivation, decreased caspase-3 and -9 expression, increased Bcl-2/Bax ratio, and activated integrin-linked kinase (ILK)-Akt; ILK-siRNA abolishment confirmed ILK-Akt as the required anti-apoptotic pathway [Zhao et al., 2011; PMID 21935929]

Row 1 is the primary peer-reviewed characterization of TB-500 as a distinct compound (Ac-LKKTETQ), establishing its chemical identity, mass spectrometric profile, and synthetic method. Row 2 characterizes the full-length 43 AA thymosin beta-4 protein in human EPC cell preparations, not the TB-500 heptapeptide fragment. The ILK/Akt data in Row 2 apply to Tβ4 (43 AA), not TB-500 (7 AA); the extent to which the Ac-LKKTETQ fragment independently activates ILK/Akt has not been established in the published peer-reviewed literature as of June 2026. No published peer-reviewed study has investigated TB-500 intranasal delivery in any model system. These observations do not constitute evidence of efficacy or safety for the TB-500 nasal spray formulation in any organism.

What are the Potential Research Applications?

In controlled laboratory environments, TB-500 nasal spray has been investigated for the following research applications. These are observed in preclinical and in vitro contexts only and do not constitute claims of efficacy or safety in any organism.

Actin Cytoskeletal Dynamics and G-Actin Sequestration Research

TB-500 (Ac-LKKTETQ) is the minimal actin-binding domain of thymosin beta-4, making it a research tool for studying G-actin sequestration at defined concentrations. Research applications include G-actin binding assays characterizing the actin-sequestration kinetics of Ac-LKKTETQ versus full-length Tβ4, actin polymerization dynamics studies in reconstituted actin systems, lamellipodia and filopodia formation assays in migrating cell preparations, and comparative studies of full-length Tβ4 versus the LKKTETQ minimal domain in matched actin-binding assay systems.

Cell Migration and Wound Healing Research

The LKKTETQ domain’s role in actin-dependent cell migration supports investigation in wound healing model systems. Research applications include wound scratch assays in endothelial cell and keratinocyte cell preparations using TB-500 as the actin-binding research tool, transwell migration assays for endothelial progenitor cell and keratinocyte chemotaxis, wound edge cytoskeletal remodeling characterization, and collagen deposition studies in fibroblast cell preparations.

Angiogenesis and Vascular Biology Research

TB-500’s actin-binding activity in endothelial cell preparations supports investigation of its role in vascular biology research. Research applications include endothelial tube formation assays (Matrigel or fibrin-based), investigation of actin-dependent endothelial cell sprouting and lumen formation, VEGF pathway interaction studies in matched endothelial cell preparations, and comparative vascular biology research contrasting TB-500 minimal domain activity versus full-length Tβ4 in the same assay systems.

Intranasal Actin-Binding Peptide Delivery Research

TB-500’s small molecular weight (~0.89 kDa), N-terminal acetylation-derived aminopeptidase resistance, and favorable nasal mucosal absorption profile at this size make it a research-relevant model compound for investigating intranasal delivery of actin-binding heptapeptides. Research applications include nose-to-brain transport characterization for acetylated heptapeptides in rodent olfactory model preparations, comparative nasal mucosal stability studies for acetylated versus non-acetylated LKKTETQ sequence forms, and intranasal pharmacokinetic profiling of TB-500 in rodent model systems.

What are the Potential Side Effects?

Researchers in preclinical and in vitro settings have noted the following observations. Long-term safety and toxicity profiles remain incompletely characterized for the research-grade nasal spray formulation.

No completed human clinical trials for TB-500 fragment (Ac-LKKTETQ): No completed, published human clinical trials have investigated the TB-500 heptapeptide fragment for any indication as of June 2026; all clinical safety data involves the full-length 43 AA thymosin beta-4 protein (e.g., RGN-259 ophthalmic formulation); this data does not transfer directly to the TB-500 fragment

• Preclinical animal safety profile – generally favorable but incompletely characterized: Preclinical animal model preparations using the thymosin beta-4 class of compounds have generally not identified acute toxicity signals; no lethal dose (LD₁) data specific to the Ac-LKKTETQ fragment has been published as of June 2026
• Actin cytoskeletal modulation via inadvertent intranasal self-exposure: TB-500 modulates G-actin availability and thereby influences cytoskeletal dynamics in exposed cells; inadvertent high-dose intranasal self-exposure carries a theoretical risk of acute actin-binding activity at nasal mucosal cells, which could transiently affect local cell motility and cytoskeletal integrity at the administration site
• Nasal mucosal irritation (local administration context): As an N-terminal acetylated heptapeptide, TB-500 may produce mild mucosal irritation at the administration site in rodent or ex vivo nasal mucosal tissue preparations; these potential effects have not been characterized in published peer-reviewed nasal administration studies
• WADA-prohibited status – performance-relevant pharmacology: The WADA-prohibited status reflects the regulatory determination that thymosin beta-4 class compounds have performance-relevant pharmacology; this does not constitute a specific safety assessment for the research-grade nasal spray formulation
• Absence of intranasal-specific safety data: No safety or tolerability data specific to the intranasal route of administration for TB-500 has been published in the peer-reviewed literature as of June 2026

No human safety or tolerability data has been established for TB-500 (Ac-LKKTETQ) nasal spray via the intranasal route. These observations are derived from experimental systems and class-level preclinical context and should not be extrapolated to human or animal outcomes.

Risk & Handling

Handling Precautions

Standard laboratory PPE is required: nitrile gloves, a laboratory coat, and eye protection. The following nasal spray-specific precautions apply:

1. Do not direct the nasal spray actuator toward the face, eyes, or mucous membranes during handling, testing, or transfer. TB-500 is an actin-binding heptapeptide that modulates G-actin sequestration and cytoskeletal dynamics in cell preparations; inadvertent intranasal self-exposure at research concentrations carries a theoretical risk of actin-binding activity in nasal mucosal cells for which no human safety data has been established.
2. Handle the nasal spray solution in a clean laboratory environment. For aliquoting or analytical sampling, use a laminar flow cabinet.
3. The nasal spray solution is an aqueous formulation susceptible to microbial contamination if compromised. Handle under aseptic conditions. Discard if the solution appears cloudy, discolored, or shows particulate matter.
4. Avoid aerosol generation during any manipulation of the nasal spray solution.

Exposure Risks

Risk Tier: LOW-MODERATE

TB-500 (Ac-LKKTETQ) has a generally favorable preclinical safety profile across thymosin beta-4 class model systems. No completed human clinical trials for the Ac-LKKTETQ fragment form have been published; safety data from full-length Tβ4 (RGN-259 topical ophthalmic) does not directly transfer to the TB-500 fragment via any route. No human safety or tolerability data has been established for TB-500 nasal spray via the intranasal route. The WADA-prohibited classification reflects performance-relevant pharmacology rather than a specific toxicological finding. Researchers should treat this compound with precautions appropriate to a biologically active actin-binding peptide with WADA-prohibited status.

Storage

In-use nasal spray: Store at 2-8°C. Use within 28 days of first actuation. Protect from light. Keep upright.

DO NOT FREEZE the ready-to-use nasal spray formulation. Freezing alters pH, buffer stability, and spray actuation properties. Repeated freeze-thaw cycles may promote TB-500 aggregation.

Lyophilized bulk stock (if applicable): Store at -20°C in sealed, desiccated, light-protected containers. Avoid repeated freeze-thaw cycles.

Discard any solution that appears cloudy, discolored, or shows visible particulate matter.

FAQs

Q: How does intranasal TB-500 access relevant research targets in preclinical models?

A: TB-500 (Ac-LKKTETQ; ~0.89 kDa) has a small molecular weight, favorable for nasal mucosal absorption via paracellular and transcellular pathways. The intranasal route bypasses hepatic first-pass metabolism, providing access to systemic circulation, where peripheral targets including wound edge endothelial cells, keratinocytes, and connective tissue fibroblasts are research-relevant – and via olfactory nerve transport to CNS targets [Wong et al., 2024; PMID 38441832]. The N-terminal acetylation provides aminopeptidase resistance at the nasal mucosa. No compound-specific intranasal pharmacokinetic or delivery data exists for TB-500. No human intranasal delivery data has been established.

Q: What is the recommended storage and in-use shelf life for TB-500 nasal spray?

A: Sealed product should be stored at 2-8°C, protected from light. Once first actuated, in-use shelf life is 28 days at 2-8°C. DO NOT FREEZE the ready-to-use solution; freezing may promote aggregation. Lyophilized bulk stock should be stored at -20°C in sealed, desiccated, light-protected conditions. Discard if the solution shows cloudiness, discoloration, or particulate matter.

Q: Is the TB-500 nasal spray formulation suitable for cell culture or in vitro assay systems?

A: The formulation is prepared in sterile PBS (pH 7.0-7.4) without preservatives, making it compatible with standard cell culture pH ranges. Dilution into culture medium before application is recommended to normalize osmolarity. Researchers should account for TB-500’s G-actin sequestration activity when designing assay systems with actin-cytoskeleton-dependent readouts – actin polymerization assays, cell migration assays, and cytoskeletal staining protocols will all be influenced by TB-500’s mechanism of action. Researchers are responsible for confirming compatibility with their specific assay system.

Q: How does TB-500 differ from full-length thymosin beta-4 (Tβ4)?

A: TB-500 (Ac-LKKTETQ; CAS 885340-08-9; MW 889.018 g/mol; 7 amino acids) is a synthetic N-terminal-acetylated heptapeptide corresponding to the actin-binding domain at residues 17-23 of Tβ4. Full-length Tβ4 (CAS 77591-33-4; MW ~4963 g/mol; 43 amino acids) is an endogenous protein with a broader biological activity profile. Published human clinical trial data – including RGN-259 (corneal wound healing) and venous ulcer studies – used full-length Tβ4, not TB-500. ILK/Akt pathway activation characterized for Tβ4 [Zhao et al., 2011; PMID 21935929] applies to the full-length 43 AA protein; this activity has not been established for the TB-500 fragment. The two molecules have different CAS numbers, molecular weights, and regulatory histories. Clinical data for Tβ4 cannot be directly applied to TB-500.

Q: What is the WADA status of TB-500?

A: TB-500 is prohibited under the 2026 WADA Prohibited List, Class S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Thymosin beta-4 and its derivatives — explicitly including TB-500 – are named under S2.3 (Growth Factors and Growth Factor Modulators). This prohibition applies both in and out of competition for all WADA Code signatories. Researchers in sport-adjacent contexts must verify current status at GlobalDRO.com. RCDbio products are supplied for laboratory research purposes only.

Q: What is the FDA regulatory status of TB-500?

A: TB-500 has no FDA-approved indication for any formulation or route. It was classified as a 503A Category 2 bulk drug substance in late 2023, then removed from Category 2 effective April 15, 2026. Both TB-500 and full-length Tβ4 are scheduled for PCAC evaluation at the July 23-24, 2026 hearing under Docket No. FDA-2025-N-6895. Removal from Category 2 does not authorize compounding; TB-500 remains unavailable for legitimate compounding until after the PCAC review and subsequent FDA rulemaking. The research-grade nasal spray supplied by RCDbio is for laboratory research use only.

Q: What is the research significance of the N-terminal acetylation in TB-500?

A: The N-terminal acetyl (Ac-) group on the leucine residue of TB-500 is a synthetic modification not present in the non-acetylated LKKTETQ sequence. It was confirmed as a defining characteristic of the TB-500 formulation by Esposito et al. (2012) using high-resolution mass spectrometry [PMID 22962027]. The acetylation provides resistance to aminopeptidase-mediated degradation at the N-terminus, extending the biological half-life of the peptide in biological fluids and at mucosal surfaces relative to the non-acetylated sequence. Researchers comparing TB-500 with native LKKTETQ or other thymosin beta-4 fragments should account for this modification when interpreting differences in actin-binding kinetics or cellular activity between acetylated and non-acetylated forms.

Related Research Compounds

Researchers investigating TB-500 nasal spray may also be interested in the following compounds currently available for laboratory research at RCDbio:

BPC-157 Nasal Spray – The stable gastric pentadecapeptide investigated for NO-system modulation, cytoprotective signaling, and vascular endothelial recruitment in preclinical rodent preparations; the most commonly paired compound with TB-500 in research stacks, operating through non-overlapping NO-system and vascular recruitment pathways complementary to TB-500’s actin-binding mechanism.

BPC-157 + TB-500 Blend Nasal Spray – The pre-formulated dual-peptide blend for concurrent investigation of BPC-157 NO-system cytoprotective signaling and TB-500 actin-binding activity in a single administration vehicle.

MOTS-c Nasal Spray– A mitochondrial-derived peptide investigated for AMPK-mediated metabolic homeostasis and cellular stress response; relevant as a complementary cellular repair and regeneration pathway research tool.

All products listed are for laboratory and research purposes only.

References

1. Esposito, S., Deventer, K., Goeman, J., Van der Eycken, J., & 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.

   https://pubmed.ncbi.nlm.nih.gov/22962027/

2. Zhao, Y., Qiu, F., Xu, S., Yu, L., & Fu, G. (2011). Thymosin beta4 activates integrin-linked kinase and decreases endothelial progenitor cells apoptosis under serum deprivation. Journal of Cellular Physiology, 226(11), 2798-2806.

   https://pubmed.ncbi.nlm.nih.gov/21935929/

3. Wong, C.Y.J., Baldelli, A., Hoyos, C.M., et al. (2024). Insulin delivery to the brain via the nasal route: unraveling the potential for Alzheimer’s Disease therapy. Drug Delivery and Translational Research, 14(7), 1776-1793.

   https://pubmed.ncbi.nlm.nih.gov/38441832/

Research Transparency Note: Reference 1 (Esposito et al., 2012; PMID 22962027) is the primary peer-reviewed scientific characterization of TB-500 as a distinct compound containing Ac-LKKTETQ; it establishes chemical identity and analytical detection strategy but does not characterize biological activity in cell or animal systems. Reference 2 (Zhao et al., 2011; PMID 21935929) characterizes the full-length 43 AA thymosin beta-4 protein in human EPC cell preparations – not the TB-500 Ac-LKKTETQ fragment; ILK/Akt data applies to Tβ4 (43 AA) only and should not be directly attributed to TB-500. Reference 3 provides class-level intranasal peptide delivery evidence in rodent model preparations. No published peer-reviewed study has directly investigated the biological activity of the TB-500 Ac-LKKTETQ fragment in vivo or via intranasal delivery as of June 2026. All mechanistic data for TB-500 at the cellular level is inferred from full-length Tβ4 studies or from the compound’s known actin-binding domain sequence; no TB-500-specific preclinical efficacy publications are available.

Disclaimer

TB-500 Nasal Spray is exclusively for laboratory research purposes. RCDbio products are not intended to diagnose, prevent, treat, or cure any disease or medical condition.

The Food and Drug Administration has not evaluated the statements on our website. This product is not approved for human or veterinary use. Researchers must comply with all applicable local, state, and federal laws and regulations governing the purchase and use of research compounds. By purchasing, you agree to our Terms and Conditions. RCDbio reserves the right to refuse sales to unauthorized individuals.

ATTENTION: All RCDbio products are strictly for LABORATORY AND RESEARCH PURPOSES ONLY. They are not intended for human consumption, veterinary use, or any other non-research application. For queries, complaints, or support, contact support@legacy.rcdbio.co