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Traumatic Brain Injury

Introducing JD-005 IV and oral

J & D Pharmaceuticals has pioneered groundbreaking formulations of intravenous (IV) and oral salicylsalicylic acid phosphatidylcholine (JD-005). These formulations merge the potential efficacy of salicylsalicylic acid with the well-established gastrointestinal (GI) safety associated with phosphatidylcholine when combined with NSAIDs. Our focus lies in addressing both acute and chronic traumatic brain injury (TBI) scenarios.

The First 24 Hours are Critical

Traumatic brain injured individuals need to be acutely treated within the first “golden” hour and in the first 24 hours there is a continued pressing need to reduce the release of toxic proteins which include cytokines as well as acetylated tau. This one hour window of opportunity is best be treated “on site” by a rapid intravenous injection of an agent that reduces the accumulation of neuroinflammatory cytokines as well as the toxic acetylated tau (ac-tau).

The figure on the left is from the following citation: Lucke-Wold B, Seidel K, Udo R, Omalu B, Ornstein M, Nolan R, Rosen C, Ross J. Role of Tau Acetylation in Alzheimer’s Disease and Chronic Traumatic Encephalopathy: The Way Forward for Successful Treatment. J Neurol Neurosurg. 2017;4(2):140.

Our Treatment Keeps the 24-hr Window Open

We believe that the acute administration of intravenous liposomal salicylsalicylic acid will reduce both cytokine release and acetylated tau. As stated in the seminal Shin/Peiper paper, “Although previous studies have reported phosphorylated tau in human TBI (Yang et al., 2017; Okamura et al., 2019; Gorgoraptis et al., 2019), these observations were beyond the first 24 h after injury, which was examined here. Importantly, independent analysis of the 24-h samples showed no increase in tau phosphorylation. Moreover, genetic in vitro and in vivo studies showed a direct neurotoxic effect of human ac-tau on neurons. Thus, our results support a critical role for tau acetylation in the acute period following brain injury, preceding any effects of tau phosphorylation.” See figure to the right.

Treatment must continue after the 24-hr period.

Subsequent treatment during the 24 hours post TBI is aimed at continued reduction of the neurological sequelae of a TBI by using oral liposomal JD-004. By monitoring the plasma level of ac-tau and maintaining a therapeutic plasma level of the active metabolite of JD-004, namely plasma salicylate, the TBI patient will receive a “personalized, customized” medical treatment. As sequelae of TBI can last a lifetime, J & D Pharmaceuticals believes oral JD-005 may be a neuroprotective agent for the lifetime of the individual.

Use of JD-004 post-TBI has been found to statistically reduce the lifetime risk of developing Alzheimer’s Disease as described in the Shin/Pieper 2017 paper. In that paper the following is found: “The relationship between JD-004 use and incidence of clinically diagnosed TBI or AD was investigated by analyzing 7.23 million United States (US) commercially insured individuals. A cohort of TBI patients taking JD-004 was compared to a matched aspirin population. After 6 years of follow-up, JD-004 usage was associated with a significantly reduced risk of clinically diagnosed TBI.”

Traumatic Brain Injury

Introducing JD-005 IV and oral

The First 24 Hours are Critical

Our Treatment Keeps the 24-hr Window Open

Treatment must continue after the 24-hr period.

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