Venomous and hematophagous animals use their venom or saliva for survival, to obtain food, and for self-defense. Venom and saliva from these animals are cocktails of bioactive molecules primarily composed of proteins and peptides. These molecules are called toxins because they cause unwanted consequences on prey. They exhibit unique, diverse, and specific biological activities that perturb normal physiological processes of their prey and host. However, the potential of toxins as inspirations for the development of therapeutic agents or pharmacological tools has also long been recognized. In addition to their small size, the exquisite selectivity and structural stability of toxins make them attractive as starting molecule in the development of therapeutic and diagnostic agents. Drug discovery and development from venomous and hematophagous animals against cardiovascular diseases have been particularly successful. Some of the notable success include antihypertensive (captopril and enalapril) and antiplatelet agents (tirofiban and eptifibatide), as well as anticoagulants (lepirudin and bivalirudin). Highlighted in this review are many venom or saliva-derived cardiovascular-active proteins and peptides of therapeutic interest, including those that are currently in preclinical stages and those that have been approved by FDA and currently in the market. The authors attempt to summarize their structure, function, mechanism of action, and development with respect to cardiovascular diseases.

: Neurological disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, amyotrophic lateral sclerosis, Huntington’s disease (HD), epilepsy, traumatic brain injury (TBI), depression and anxiety are responsible for thousands of deaths worldwide every year. With the increase in life expectancy, there has been a rise in the prevalence of these disorders. Age is one of the major risk factors for these neurological disorders and with the aged population is set to rise to 1.25 billion by 2050. There is a growing concern to look for new therapeutic molecules to treat age-related diseases. Caffeic acid phenethyl ester (CAPE) is a molecule obtained from a number of botanical sources such as the bark of conifer trees as well as propolis which is extracted from beehives. Though CAPE remains relatively unexplored in human trials, it possesses antioxidant, anti-inflammatory, antimitogenic and anti-cancer activities as shown by preclinical studies. Apart from this, it also exhibits tremendous potential for the treatment of neurological disorders through modulation of multiple molecular pathways and attenuation of behavioural deficits. In the present article, we have reviewed the therapeutic potential of CAPE and its mechanisms in the treatment of neurological disorders.

Background: Chemotherapy-induced peripheral neuropathy is a debilitating pain syndrome produced as a side effect of antineoplastic drugs like paclitaxel. Despite efforts, the currently available therapeutics suffer from serious drawbacks like unwanted side effects, poor efficacy and provide only symptomatic relief. Hence, there is a need to find new therapeutic alternatives for the treatment of Chemotherapy-induced peripheral neuropathy. Objective: The objective of this study was to explore the protective potential of Caffeic acid phenethyl ester in paclitaxel-induced neuropathic pain. Methods: We examined the effects of Caffeic acid phenethyl ester by administering Paclitaxel (2 mg/kg, intraperitoneal) to female Sprague Dawley rats on four alternate days to induce neuropathic pain, followed by the administration of Caffeic acid phenethyl ester (10 and 30 mg/kg, intraperitoneally). Results: Rats that were administered paclitaxel showed a substantially diminished pain threshold and nerve functions after 28 days. A significantly increased protein expression of Wnt signalling protein (β-catenin), inflammatory marker (matrix metalloproteinase 2) and a decrease in endogenous antioxidant (nuclear factor erythroid 2–related factor 2) levels were found in paclitaxel administered rats in comparison to the naïve control group. Caffeic acid phenethyl ester (10 and 30 mg/kg, intraperitoneal) showed improvements in behavioural and nerve function parameters along with reduced expression of β-catenin, matrix metalloproteinase 2 and an increase in NF-E2–related factor 2 protein expression. Conclusions: The present study suggests that Caffeic acid phenethyl ester attenuates chemotherapy-induced peripheral neuropathy via inhibition of β-catenin and matrix metalloproteinase 2 and increases nuclear factor erythroid 2–related factor 2 activation.

Cancer is a genetic disease caused due to mutations in the tumor suppressor genes or oncogenes involved in the cell cycle regulation. It may include mutations that may be inherited or acquired during one’s lifetime and affect single gene or multiple genes, chromosomes and their protein expression patterns, ultimately leading to a loss of control over the cell cycle and culminating in uncontrolled cell growth. With the tremendous increase in global cancer burden and early detection being the key to cure, it has become imperative that the genes be studied and new genetic and biochemical testing techniques be utilized. In this review, we have looked at various mutations involved in common cancer-causing genes, their role under normal physiological conditions, mechanisms of mutation and their occurrence in different types of cancers. Also, the review focuses on conventional and novel approaches for genetic and biochemical testing, the techniques used and their advantages and limitations.