Phase 1 Trial Finishes Dosing 1st AML Patient Group With Actimab-A Plus Venclexta

Phase 1 Trial Finishes Dosing 1st AML Patient Group With Actimab-A Plus Venclexta

The first group of patients with relapsed or refractory acute myeloid leukemia (AML) has been dosed in a Phase 1/2 dose-escalation trial assessing the safety and efficacy of Actimab-A and Venclexta (venetoclax) as a combination therapy, Actinium Pharmaceuticals announced.

Participants receiving the lowest dose of Actinium’s Actimab-A (0.50 microcurie (uCi)/kg) have completed treatment and cleared their first safety evaluation. These patients will start receiving a higher dose (1.0 uCi/kg), which will continue to be given alongside Venclexta.

This Phase 1/2 trial (NCT03867682), which is still recruiting participants at the University of California and University of Louisville in the U.S., aims to demonstrate that Actimab-A can improve Venclexta’s therapeutic efficacy in a clinical setting.

If proven, these findings will confirm previous preclinical observations presented last year at the American Association for Cancer Research Annual Meeting that showed Actimab-A can help Venclexta destroy cancer cells by lowering the levels of a protein, called MCL-1, that allows them to become resistant to Venclexta.

“We are pleased to confirm that the second combination trial in our CD33 program is advancing through the dose escalation study as planned,” Mark Berger, MD, chief medical officer at Actinium, said in a press release. “Despite approval in multiple blood cancers, including AML, most AML patients are not cured with venetoclax regimens and eventually relapse. Based on the preclinical data, synergy with venetoclax and Actimab-A should lead to higher remission rates in R/R AML.”

“We expect to complete the proof of concept Actimab-A venetoclax combination trial in 2021,” Berger said.

Developed and marketed by Genentech and AbbVie, Venclexta is an oral small molecule inhibitor of BCL-2 — a protein that is overproduced by cancer cells and prevents them from being destroyed by anti-cancer therapies. By blocking the activity of BCL-2, Venclexta can trigger signaling mechanisms leading to cancer cell death.

Despite its success treating some forms of AML, Venclexta cannot block the activity of MCL-1, one of the members of the BCL-2 protein family, which restricts its effectiveness.

This limitation may potentially be surpassed by combining the therapy with Actimab-A, a radioimmunotherapy that is made up of an antibody targeting CD33 — a protein receptor found on the surface of AML cells — coupled with a radioactive substance. Once the antibody binds to its target on AML cells, a large amount of radiation is released onto them.

By delivering large amounts of radiation directly to cancer cells and curbing their resistance to Venclexta by lowering their MCL-1 levels, Actimab-A is thought to boost Venclexta’s therapeutic efficacy.

The Phase 1/2 trial that is now evaluating if this synergistic relationship between Actimab-A and Venclexta exists in a clinical setting will be divided into two phases: an initial phase that will attempt to determine the maximum tolerated dose of Actimab-A that can safely be given alongside Venclexta; and a second phase that will determine the percentage of patients who responded to the combination therapy within a period of six months without receiving any other form of AML treatment.

Enrollment is opened to adult patients with CD33-positive relapsed or refractory AML who were previously treated with Venclexta, as well as for those who never received the medication. More details about the study can be found here.

In addition to this study, another Phase 1 trial (NCT03441048) is currently evaluating the safety and efficacy of Actimab-A combined with CLAG-M chemotherapy (cladribine, cytarabine, G-CSF, and mitoxantrone) in patients with relapsed or refractory AML. Preliminary data from this study showed the addition of Actimab-A to CLAG-M increased the percentage of patients who entered remission by nearly 60% compared to CLAG-M alone, demonstrating Actimab-A’s potential to increase the effectiveness of other therapies.