Actinogen reveals new data to salvage depression drug xanamem after phase 2 failure

Earlier this month, Actinogen Medical faced a setback when its cortisol-blocking drug, xanamem, failed to meet the primary endpoint in a phase 2 trial aimed at improving attention and memory in patients with cognitive dysfunction and major depressive disorder. However, the Australian biotech company recently announced more promising secondary results related to depression.

On August 26, Actinogen revealed that patients who took 10 mg of xanamem daily for 10 weeks reported feeling less depressed compared to those who received a placebo. Additionally, these patients exhibited a 50% higher rate of depression remission, highlighting the drug’s potential in alleviating depressive symptoms. The trial also confirmed earlier findings showing that xanamem effectively reduced the severity of depression, further supporting its potential as a novel anti-depressant.

Dr. Steven Gourlay, CEO of Actinogen, expressed optimism about the results, stating, “This trial confirms our conclusion that a 10 mg daily dose of xanamem is clinically active in the brain and has the potential to be an effective anti-depressant with a novel mechanism.” He emphasized xanamem's competitive edge in the crowded antidepressant market, citing its favorable safety profile and the enduring benefits observed in the trial.

Following the announcement, Actinogen’s stock price surged by approximately 90%, recovering from a significant 60% drop that occurred two weeks earlier when the initial phase 2 trial results were released. This rebound underscores the positive impact of the secondary endpoints on investor confidence.

Beyond its potential in treating depression, xanamem is currently being tested in a phase 2 trial for Alzheimer’s disease. Unlike the depression trial, the study for Alzheimer’s will not include the attention and memory tests that xanamem initially failed. This strategic decision aims to better assess the drug’s effectiveness in treating Alzheimer’s without the confounding factors from previous endpoints.

Xanamem works by inhibiting the activity of the 11β-HSD1 enzyme, which is crucial in the production of the stress hormone cortisol. Elevated levels of cortisol are known to negatively impact cognitive function, making xanamem’s mechanism of action particularly relevant for a range of neurological and psychiatric conditions. Actinogen is also exploring the potential of xanamem in treating Fragile X syndrome and other related disorders.

In summary, while Actinogen’s xanamem did not meet the primary cognitive function endpoint in its recent phase 2 trial, the drug showed significant promise in treating depression. Patients on xanamem experienced reduced depressive symptoms and higher rates of remission compared to those on placebo. These findings have provided a much-needed boost to Actinogen’s stock price and have opened up new avenues for the drug’s application in other neurological and psychiatric conditions.