Licence marks Atara as a new cell therapy contender

At first glance yesterday’s 17% climb in Atara Biotherapeutics shares looks surprising; all the young biotech did was formalise a $4.5m licence with Memorial Sloan-Kettering (MSK) that had already been negotiated earlier.

Still, perhaps the rise had more to do with investor realisation of what Atara had achieved, almost in stealth mode, before floating on Nasdaq last October. One of the allogeneic T-cell projects in yesterday’s licence is already in US practice guidelines and has breakthrough status, putting Atara with Juno and Novartis as the only three cell therapy companies to hold this accolade.

Juno and Novartis’s breakthrough designations relate to their respective CAR-T projects, JCAR015 (also licensed from MSK) and CTL019. Meanwhile, that attached to MSK/Atara relates to EBV-CTL – allogeneic T cells specific for Epstein-Barr virus (EBV) antigens, for use against EBV-associated lymphoproliferative disorder, a rare but deadly complication of allogeneic stem cell transplantation.

Even more surprising than yesterday’s 17% rise is the fact that Atara was not founded with this project in mind; rather it was to develop the molecularly targeted Amgen assets PINTA 745, STM 434 and ATA 842. But last September it negotiated a licence to three MSK projects: EBV-CTL, as well as T cells activated against cytomegalovirus and WT1.

The relevance of EBV to oncology is well documented, and the virus is known to be associated with certain lymphomas and nasopharyngeal carcinoma. While most people develop adaptive immunity to EBV after a childhood infection, viral reactivation can occur later in life, possibly because of immune system impairment.

Thus the UK’s Cell Medica is taking advantage of the presence of EBV antigens on the cancer cells of patients with NK/T-cell lymphoma, attempting to target these with autologous activated T cells (Interview – UK’s Cell Medica looks to confirm T-cell therapy hopes, November 28, 2014).

Meanwhile, at last year’s ASH meeting Dr Sara Ghorashian from University College London presented data on the use of EBV-infected B cells to stimulate T cells expressing a CD19-directed CAR, though for various reasons these results underwhelmed.

EBV-associated lymphoproliferative disorder, the target for EBV-CTL, is another complication resulting from EBV reactivation, and untreated transplant recipients who develop it live for just 31 days on average. Standard treatment is off-label Rituxan, and gives durable remissions in 25-80% of patients.

EBV-CTL is being studied in Rituxan-refractory patients. The concept involves taking blood from donors, isolating T cells and sensitising them to EBV antigens, before enriching the cells for EBV specificity; this has resulted in a bank of 330 donor-derived EBV-specific T-cell lines at MSK, available for off-the-shelf use based on partial matching with the recipient.

Funds raised

Atara’s October IPO raised $56m, and a $66m secondary was completed just four months later. Since floating Atara stock is up 428%, though it is off its April peak, when data at the AACR showed a 63% response rate to EBV-CTL and suggested that partial responders could undergo additional cycles of cells from the same donor, and non-responders with a different cell line.

The risk, of course, is that the niche nature of EBV-associated lymphoproliferative disorder will render Atara’s sales negligible, especially since MSK already makes EBV-CTL available to patients.

But the promise is that EBV-CTL is an important first step to validate Atara’s cell therapies, pointing to further pipeline projects; the group even moots the possibility of licensing CAR-T assets from MSK.

For now, the off-the-shelf nature of EBV-CTL implies speed and convenience in a setting where moving fast is essential, and the cells’ recommendation under NCCN guidelines in this setting, together with breakthrough designation, suggests a quick path to market.

It is basically down to Atara to commercialise a project that MSK has developed.

To contact the writer of this story email Jacob Plieth in London at [email protected] or follow @JacobPlieth on Twitter

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