Further development is needed regarding the toxicity of these materials in both biological and environmental environments, in the short and long terms, for these applications to be find more brought into widespread use. We refer the reader to recent reviews on the use of carbon nanotubes and fullerenes in biology and medicine
[5, 6, 51]. Typically, non-functionalized carbon-based nanomaterials are considered to be toxic, but significant work has been done to make these structures soluble and biocompatible. For example, it has been demonstrated that C60 fullerene with five cysteine residues attached to its surface is water soluble and does not cause cellular toxicity [34]. As with any drug lead, to move from an idea to a marketable drug can take between 10 to 15 years. Therefore, significant research effort is required to develop this theoretical [Lys]-fullerene design
into a drug for therapeutic use. Future simulations are required to determine whether these compounds are potent blockers of mammalian Nav channels and if they are specific to a particular channel sub-type. Following this, experiments would need to be SIS3 price performed to confirm theoretical findings and determine toxicity profiles. Polypeptide toxins from venomous animals have evolved over millions of years, aimed at rapidly immobilizing and capturing prey. Since they act on a broad spectrum of ion channel families and are rapidly degraded in vivo, converting these toxins to drugs represents a considerable challenge, and attempts are being made to synthesize smaller and more durable mimetic structures [1–4]. The use of nanomaterials, which replace the rigid backbone of the naturally occurring toxins, Montelukast Sodium may prove to be a fruitful approach for such an endeavor. In the past, fullerenes suffered from high production costs which generated an obstacle to the development of fullerene-based applications, but the cost has rapidly declined [5]. Conclusions Voltage-gated sodium channels are present throughout muscle and neuronal cells in mammals. Their PU-H71 in vitro dysfunction has
long been linked to disorders such as epilepsy and chronic pain. Toxins from venomous species such as cone snails and scorpions have demonstrated activity against sodium channels. One example is the polypeptide toxin μ-conotoxin (PIIIA), extracted from the cone snail, which has been shown to potently block both bacterial and mammalian Nav channels [16, 17, 52]. Unfortunately, converting toxins to drugs represents a considerable challenge [1–4]. We attempt to mimic the structure of μ-conotoxin by (1) replacing its bulky core with a C84 fullerene and (2) chemically attaching positively charged groups to the fullerene surface. Although fullerenes have previously been identified as possible ion channel blockers [10–15], no studies have demonstrated the potential of designing fullerenes through chemical modification to target specific ion channels.