Leronlimab is a novel humanized monoclonal antibody that is a CCR5 antagonist with the potential for multiple therapeutic indications, including a therapy for treating Covid-19 Patients. Leronlimab targets and binds to the CCR5 receptor and, for example, inhibits RANTES (CCL5 found in high levels in severe to critical Covid-19 patients) from binding to CCR5 and thereby preventing the formation of chemokines and cytokines that cause the “cytokine storm” which invades the lungs causing severe inflammation and reductions in blood-oxygen levels.
Cytodyn Inc., located in Vancouver, Washington, is a late-stage biotechnology company developing leronlimab.
CytoDyn’s Phase 2b/3 trial to evaluate the efficacy and safety of leronlimab for patients with severe-to-critical COVID-19 indications is a two-arm, randomized, double blind, placebo controlled, adaptive design multicenter study. Patients are randomized to receive weekly doses of 700 mg leronlimab, or placebo. Leronlimab and placebo are administered via subcutaneous injection. The study has three phases: Screening Period, Treatment Period, and Follow-Up Period. The primary outcome measured in this study is: all-cause mortality at Day 28. Secondary outcomes measured are: (1) all-cause mortality at Day 14, (2) change in clinical status of subject at Day 14, (3) change in clinical status of subject at Day 28, and (4) change from baseline in Sequential Organ Failure Assessment (SOFA) score at Day 14.
On October 20, 2020, Cytodyn announced recommendations from the independent Data Safety Monitoring Committee (DSMC) following its review of the interim analysis of the Company’s Phase 2b/3 registrational trial in patients with severe-to-critical COVID-19. The interim analysis was performed on data from the first 195 (50%) of 390 planned patients. The DSMC recommended that the trial continue without modification to achieve the primary endpoint and requests another interim analysis when enrollment reaches 75% level (or 293 patients) to review patient mortality and other clinical outcome data between the two study arms (leronlimab vs. placebo).
Endocrinologist at Boston Children’s Hospital and Harvard Medical School, David Ludwig, MD, PhD presents a groundbreaking diet program that debunks the myth that calorie balance is the key to weight loss and teaches readers how to reprogram their fat cells to lose weight without counting calories or feeling hungry.
GenSpera’s first drug, G-202, targets PSMA Enzyme, found on the walls of the blood vessels that feed cancer tumors, regardless of the type of cancer. G-202 is currently in phase 1 safety trials at the University of Wisconsin Carbone Cancer Center (Madison, Wisconsin), the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University School of Medicine, and the Cancer Therapy & Research Center at the University of Texas Health Science Center of San Antonio, at San Antonio, Texas.
At the completion of this multi-center trial, GenSpera expects to move on to Phase 2 trials possibly in prostate, stomach and other cancers, all with the same drug, G-202.
In the case of GenSpera’s second drug, G-115, its target is PSA, an enzyme found only in prostate cancer tumors.
Should we not challenge all assumptions? I never once questioned the conventional wisdom [. . . about the pathology of diabetes]. I actually assumed the pathological sequence was settled science.
You can think of insulin as this master hormone that controls what our body does with the food we eat; whether we burn it or store it. It’s called fuel partitioning in the lingo? Insulin resistance is when cells become increasingly resistant to insulin trying to do its job.
Is conventional wisdom failing me and everyone else?
Most people believe that obesity is the cause of insulin resistance? What if we have it backwards? Is it possible that insulin resistance causes obesity? The implication is profound. What if obesity — that is, the storing of fat — is a coping mechanism to insulin resistance? How much better would we be to treat the cause rather than the effect?
Despite eating well and exercising often, Peter Attia himself began to gain weight. He developed metabolic syndrome, a pre-cursor to diabetes in which a person becomes insulin resistant. He started to question the assumptions he and the majority of the medical community made about diabetes. He wondered: could it be that insulin resistance caused obesity and not the other way around? Could it be that, in the same way a bruise forms in order to protect the body after an injury, that gaining weight is a coping mechanism for a deeper problem at the cellular level?
“What if we’re fighting the wrong war—fighting the obesity rather than insulin resistance?