TAT-CBD3 - 10ml/400mg - Spray

ADVANCED DELIVERY SYSTEM - CELL PENETRATING PEPTIDE TECHNOLOGY

This product utilizes advanced delivery technology incorporating calibrated cell-penetrating peptide (CPP) systems. The formulation is engineered to support efficient and targeted intracellular delivery of active ingredients, contributing to enhanced transport performance and bioavailability.

SPECIFICATIONS

Product Code: TC3400D

Sequence: H-Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Ala-Arg-Ser-Arg-Leu-Ala-Glu-Leu-Arg-Gly-Val-Pro-Arg-Gly-Leu-OH

Molecular Formula: C134H243N59O32

Molecular Weight: 3192.73 g/mol

CAS: 1355359-36-2

Purity: Technical / Research Grade ≥98%

Other details: No TFA Salt

Form: Liquid Solution

Color: Clear / Slightly opalescent

Total Content: 10 mL / 400 mg

Concentration: 40 mg/mL

Approximate Sprays per Bottle: ~82

Approximate Peptide per Spray: ~4,88 mg

Vehicle / Carrier System: Proprietary carrier system

Storage Temperature: 4°C (Do not freeze)

Source: Synthetic

Safety classification: Standard handling

DESCRIPTION

TAT-CBD3 is a synthetic peptide designed to modulate key molecular mechanisms involved in neuropathic pain, a complex and often chronic condition arising from dysfunction or damage to the nervous system.

The CBD3 sequence is derived from a functional domain of CRMP-2 (collapsin response mediator protein-2), a protein known to regulate voltage-gated calcium channels, particularly CaV2.2, which play a central role in nociceptive signal transmission. The peptide is conjugated with the TAT (trans-activator of transcription) cell-penetrating domain, enabling efficient intracellular delivery into sensory neurons.

Neuropathic pain is frequently characterized by hyperexcitability of primary sensory neurons, leading to exaggerated responses to stimuli, spontaneous pain signaling, and persistent sensitization of neural pathways. A major contributor to this pathological state is the dysregulation of calcium influx through membrane-bound ion channels. Activation of these channels facilitates the release of excitatory neurotransmitters, amplifying pain transmission within the peripheral and central nervous system.

TAT-CBD3 acts by disrupting the interaction between CRMP-2 and CaV2.2, a process that normally enhances calcium channel trafficking to the neuronal membrane and increases channel activity. By interfering with this interaction, the peptide:

• Reduces the functional expression of CaV2.2 channels at the cell surface
• Decreases calcium influx into presynaptic terminals
• Limits the release of excitatory neurotransmitters
• Attenuates synaptic transmission within nociceptive pathways

In addition to its effects on N-type calcium channels, experimental evidence indicates that TAT-CBD3 also reduces T-type calcium currents, which are known to contribute to increased neuronal excitability following nerve injury.

The combined effect of these actions is a reduction in nociceptor hyperexcitability and a modulation of abnormal pain signaling. In preclinical models, this has been associated with improvements in key features of neuropathic pain, including mechanical hypersensitivity, cold sensitivity, allodynia, and hyperalgesia.

Unlike conventional analgesics, which often act through broad and non-specific mechanisms, TAT-CBD3 represents a more targeted approach based on selective interference with protein–protein interactions involved in pain transmission. This allows modulation of calcium channel activity without complete channel blockade, potentially reducing the risk of adverse effects associated with direct CaV2.2 inhibition.

The therapeutic relevance of this approach is supported by the central role of CaV2.2 in chronic pain pathways. While direct channel blockers can produce potent analgesia, their clinical use is limited by systemic side effects due to widespread physiological roles of calcium channels. Targeting regulatory mechanisms such as the CRMP-2/CaV2.2 interaction offers an alternative strategy aimed at achieving analgesic effects with improved specificity.

Preclinical studies have demonstrated that TAT-CBD3 can significantly reduce pain-related behaviors in multiple models of inflammatory and neuropathic pain, although responses may vary depending on the underlying pathology. Modifications of the CBD3 sequence have also been shown to enhance binding efficiency and analgesic efficacy in certain models, supporting ongoing optimization of this peptide class.

Overall, TAT-CBD3 represents a novel neuromodulatory approach focused on regulating calcium channel function rather than directly inhibiting it, making it a valuable tool in the study of chronic pain mechanisms and a potential foundation for next-generation targeted analgesic strategies.

DISCLAIMER

This product is intendend for lab research and development use only. These studies are performed outside of the body. This product is not medicines or drugs and has not been approved by the FDA or EMA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals.

All product information provided on this website is for informational and educational purposes only.