European Hematology Association (EHA) 2026 Congress | iPharmaCenter

ABBVIE

AbbVie shares nine‑year CLL14 results for Venetoclax regimen in previously untreated chronic lymphocytic leukemia

AbbVie has reported final nine‑year data from the Phase 3 CLL14 study, which evaluated a fixed‑duration combination of Venetoclax and obinutuzumab in previously untreated adults with chronic lymphocytic leukemia (CLL) who had relevant coexisting conditions.

Long-term efficacy and time to next treatment

CLL14 compared Venetoclax plus obinutuzumab with chlorambucil plus obinutuzumab in patients with untreated CLL and additional comorbidities, such as higher Cumulative Illness Rating Scale scores or reduced renal function. Treatment with Venetoclax was given for a total of 12 months alongside six cycles of obinutuzumab, providing a predefined, fixed‑duration approach rather than continuous therapy.

After a median follow‑up of around 9 years, the Venetoclax combination continued to show a clear progression‑free survival advantage over the chlorambucil‑based regimen.

• Median progression‑free survival was reported at 6.4 years in the Venetoclax plus obinutuzumab arm versus 3.2 years with chlorambucil plus obinutuzumab

• The final analysis also documented a median time to next treatment of 7.6 years for patients who received the Venetoclax regimen, underscoring the durability of disease control after completion of the one‑year course.

Safety profile over extended follow-up

The nine‑year assessment indicated that the safety profile of Venetoclax in combination with obinutuzumab remained in line with earlier reports from the study. The most common grade 3 or higher adverse events observed in patients treated with the Venetoclax‑based regimen included neutropenia, thrombocytopenia, infusion‑related reactions, anemia, febrile neutropenia, pneumonia and leukopenia.

CLL context and treatment needs

Chronic lymphocytic leukemia is one of the most frequently diagnosed leukemias in adults and arises from abnormal lymphocytes that develop in the bone marrow. Many patients experience relapsed disease after an initial response, while others develop refractory disease when the cancer no longer responds to current therapy, which can necessitate multiple lines of treatment over time.

Although outcomes have improved with targeted agents, patients and clinicians still face challenges related to treatment duration, cumulative toxicity and ongoing disease monitoring.

About Venetoclax and its mechanism of action

Venetoclax is an oral, first‑in‑class small molecule that selectively targets the B‑cell lymphoma 2 (BCL‑2) protein, a key regulator that can help leukemia and other blood cancer cells evade programmed cell death.

By inhibiting BCL‑2, Venetoclax is designed to restore the normal apoptotic process, promoting the elimination of malignant cells in BCL‑2‑dependent malignancies. The medicine is being developed through a long‑standing collaboration between AbbVie and Roche and is co‑commercialized with Genentech, a Roche company, in the United States and by AbbVie in markets outside the United States.

Venetoclax is approved for multiple blood cancer indications and is available in more than 80 countries worldwide.

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JOHNSON AND JOHNSON

Imaavy shows early and sustained hemoglobin gains in pivotal study for warm autoimmune hemolytic anemia

Johnson & Johnson has released full Phase 2/3 data from the ENERGY trial of Imaavy (nipocalimab) in adults with warm autoimmune hemolytic anemia, a rare antibody mediated condition that currently lacks approved treatment options in the United States. The results indicate that the investigational neonatal Fc receptor blocker can deliver a rapid rise in hemoglobin and maintain that benefit over 24 weeks compared with placebo in patients with active disease.

Primary endpoint: stringent definition of durable hemoglobin benefit

ENERGY is a multinational, randomized, double blind, placebo-controlled study that enrolled adults with primary or secondary warm autoimmune hemolytic anemia who remained symptomatic or insufficiently controlled on standard therapies.

Participants were assigned to one of two nipocalimab dosing regimens or to placebo, on top of stable background treatment, for a 24 week blinded period followed by an open label extension.

The main objective was to determine how many patients achieved a sustained improvement in hemoglobin under a strict composite definition.

To qualify as a durable responder, a patient had to show all of the following: at least a 2 gram per deciliter increase from baseline; an absolute hemoglobin level of 10 grams per deciliter or higher; these thresholds met at a minimum of three separate visits spanning at least 28 days, starting no later than week 16; and no use of rescue interventions or escalation of background warm autoimmune hemolytic anemia therapy during that time.

• In the higher dose group receiving 30 milligrams per kilogram of Imaavy, roughly three times as many patients reached this durable hemoglobin endpoint by week 24 compared with placebo.

• A mean rise in hemoglobin of about 1 gram per deciliter was already apparent at week 1 in the active treatment arm, while the placebo group showed essentially no early change.

• By the end of the double-blind phase, close to two thirds of patients in the 30 milligram per kilogram cohort met commonly accepted clinical targets of both an absolute hemoglobin level of at least 10 grams per deciliter and an increase of 2 grams per deciliter or more above their starting value.

Fatigue improvement and steroid sparing

The trial also assessed outcomes that are highly relevant to daily life for patients with warm autoimmune hemolytic anemia, including tiredness and reliance on corticosteroids.

Nipocalimab and its mechanism of action

Nipocalimab is a high affinity monoclonal antibody that targets the neonatal Fc receptor, a transport protein that protects immunoglobulin G antibodies from degradation and prolongs their circulation time. By blocking this receptor, Imaavy is designed to lower levels of circulating immunoglobulin G, including the pathogenic autoantibodies that tag red blood cells for destruction in warm autoimmune hemolytic anemia.