Biostax Corp. Signs Collaboration Agreement with Immgenuity, Inc. to Pursue Remission in HIV - Seite 2

“Based upon existing HIV data surrounding both JKB-122 and Lodonal we believe that by performing combined research we will generate additional compelling data, that complements our existing clinical data," said Noreen Griffin, Biostax’s CEO. "We are delighted to enter into this partnership that will further develop our product candidates for the treatment of patients with HIV.”

Clinical Program JKB-122 and Lodonal

Biostax will also look to fast track a Phase 2b trial with the FDA: “Effects of JKB-122 and Lodonal on T-Cell Immune Activation and Inflammation in Non-Responders or who are Failing their CAR-T therapy with HIV.” The primary end point is to show a decrease in comorbidities and opportunistic infection and clinical symptoms such as diarrhea, fatigue, pain, upper respiratory infections, skin disorders, and confirm changes of T-cell immune activation and reduction inflammation biomarkers.

Prior clinical trials have shown Lodonal and JKB-122 can modulate the immune system by increasing NK cells, CD4, improve the CD4/CD8 and reduce opportunistic infection and pain in HIV patients while reducing inflammation. The success in these trials will provide evidence for the use of Lodonal and/or JKB-122 as part of combined therapy for remission and immune restoration in HIV patients.

About Lodonal and JKB-122

Biostax has developed a rapid release oral formulation of the drug substance “low dose naltrexone”, known as Lodonal, for use as an active immunotherapy drug with anti-inflammatory properties. Lodonal is one of the first drugs approved to be taken once-a-day as an immune system regulator for the management of HIV/AIDS. The approval by NAFDAC was based on the results of a bridging trial that resulted in a 44% increase in CD4 Count versus an 11% increase for standard of care patients.

Unlike “single target” immune suppressors, or drugs that require a specific cell receptor to act, Lodonal and JKB-122’s molecular structure allows it to be a promiscuous antagonist of various classes of receptors/proteins (multiple targets), eliciting multiple complimentary effects. Beyond modulation of the cell cycle by way of growth factor-like activities downstream of opioid receptors, clinical trials indicated that it reduces the overall activation state (metabolic shift) of cells responsive to pathogen signals, damage signals, or both (drivers of inflammation).