CBD is a naturally occurring cannabinoid constituent of cannabis. It was discovered in 1940 and is known to exhibit neuroprotective properties in many experimental systems. However, development of CBD as a drug has been confounded by the following issues:


low potency


a large number of molecular targets


marginal pharmacokineticproperties


designation as a schedule 1controlled substance


To date there has been only one cannabidiol based medicament, Epidiolex™, approved for use in humans by the U.S. Food and Drug Administration (“FDA”). The drug, Epidiolex™, is used to treat seizures due to certain medical conditions (such as Lennox-Gastaut syndrome, Dravet syndrome). It is not known how this medication works for these seizures. Cannabidiol belongs to a class of drugs known as cannabinoids. Additionally, the FDA’s Office of Orphan Products Development (“OOPD”) has designated cannabidiol eighteen (18) times since 2013 for a multitude of diseases ranging from rare forms of epilepsy to prevention of reperfusion injury due to organ transplantation to glioblastoma multiforme to autoimmune hepatitis. While the Company’s primary indications of OHE and CIPN have not been targeted by CBD-based or CBD-derived drugs and cleared by the FDA or other foreign regulatory agency, neither have the aforementioned eighteen orphan designated indications targeted by cannabidiol.

Kannalife’s present work has compared the properties of CBD with our patented novel cannabidiol derived molecule, KLS-13019, that has structural similarities to CBD. The design strategy for KLS-13019 was to increase hydrophilicity while optimizing neuroprotective potency against oxidative stress toxicity relevant to hepatic encephalopathy. In early pre-clinical studies, the responses of CBD and KLS-13019 were compared in dissociated rat hippocampal cultures in a pre-clinical model for overt hepatic encephalopathy (“OHE”) and chemotherapy induced peripheral neuropathy (“CIPN”).

Cannabinoid Therapeutics by the Numbers


Comparisons between CBD and KLS-13019 have been published in peer reviewed articles in ACS Medicinal Chemistry Letters (2016, 7, 424-428) “Discovery of KLS-13019, a Cannabidiol-Derived Neuroprotective Agent, with Improved Potency, Safety, and Permeability” and Journal of Molecular Neuroscience (14 August 2018) “Pharmacological Comparisons Between Cannabidiol and KLS-13019.” In both the ACS and JOMN papers, the protective responses of CBD and KLS-13019 were compared in dissociated rat hippocampal cultures co-treated with toxic levels of ethanol and ammonium acetate. This comparison revealed that KLS-13019 prevented neuronal toxicity from the combined toxin treatment, while both compounds exhibited complete protective efficacy back to control values.

We have made significant improvements in the chemistry efficacy and safety of our CBD-like molecules, lead by KLS-13019, that are up to 200X more potent, 10X more bioavailable, 5X safer and 1000 times more effective than CBD.

Kannalife received a grant from National Institute of Drug Abuse (NIDA) to compare CBD and our novel molecule KLS-13019 for its development in Chemotherapy Induced Peripheral Neuropathy and Drug Dependence.  CIPN is a neurodegenerative condition that afflicts patients undergoing chemotherapy with symptoms that include numbness, tingling, and pain and affects approximately 1/3 of patients undergoing chemotherapy cancer treatment. KLS-13019 can also be valuable as a potential alternative for opioid pain management.

Kannalife’s peer-reviewed research was once again published in the Journal of Molecular Neuroscience (10 May 2019) “Knockdown siRNA Targeting the Mitochondrial Sodium-Calcium Exchanger-1 Inhibits the Protective Effects of Two Cannabinoids Against Acute Paclitaxel Toxicity.” This paper compared CBD and our leading target drug candidate, KLS-13019 to produce a clear understanding of its mechanism of action.  We have focused on the treatment of chemotherapy induced peripheral neuropathy (CIPN) and other oxidative stress related disorders involving chronic pain managament and neurodegeneration.


We are in the leadership role as a commercial drug discovery company advancing cannabinoid therapeutics to successfully synthesize CBD derived new chemical entities.

Intellectual Property

We have synthesized, pre-clincally tested and patented our proprietary CBD derived new chemical entities (“NCEs”), including KLS-13019 and also formulated a new CBD based molecule, KLS-13023. KLS-13019 is our lead target drug candidate and is part of an estate of new chemical entities (“NCEs”) underlying U.S. Patent 9,611,213 titled “Functionalized 1,3 Benzene-diols and their Method of Use for the Treatment of Hepatic Encephalopathy”. This patent is part of a divisional patent application by the Company to the USPTO whereby the Company sought separate claims for composition of matter, covered in Pat. 9,611,213 and separate claims for method of treatment; and U.S. Patent 10,004,722 titled “Method for Treating Hepatic Encephalopathy or a Disease Associated with Free Radical Mediate Stress and Oxidative Stress with Novel Functionalized 1,3 Benzene-diols.”

KLS-13019 and its related molecules describe novel functionalized 1,3-benzenediols (“Cannabidiol Derived Molecules”) and methods that may be useful and have potential for the treatment of hepatic encephalopathy and related conditions. The present invention further describes a novel chemotype that may be useful and have potential for the treatment of diseases associated with hepatic encephalopathy. The present invention further describes a novel chemotype that may be useful and have potential as neuroprotective agents. The Cannabidiol Derived Molecules under the present invention may be useful and have potential for treating and preventing diseases associated with free radical mediated stress and oxidative stress including, for example, as previously mentioned, hepatic encephalopathy, Parkinson’s disease, Alzheimer’s, Huntington’s disease, traumatic head injury, stroke, epilepsy, neuropathic pain, Chronic Traumatic Encephalopathy (CTE), Post Cardiac Arrest Hypoxic Ischemic Encephalopathy, and Epileptic Encephalopathy.