News in brief: Tecartus CAR T-cell therapy licensed for R/R MCL; Physicians stay clear of social media; Drugs for platelet-mediated thrombosis may be re-targeted for COVID-19 treatment


Tecartus CAR T-cell therapy licensed for R/R MCL

The CAR T-cell therapy brexucabtagene autoleucel (Tecarta) has been licensed in Australia for use in patients with relapsed or refractory Mantle Cell Lymphoma.

According to the product information approved by the TGA, the Gilead product is a CD19 directed genetically modified autologous T cell immunotherapy.

A patient’s T cells are harvested and genetically modified ex vivo by retroviral transduction to express a chimeric antigen receptor (CAR) comprising a murine anti-CD19 single chain variable fragment (scFv) linked to CD28 and CD3-zeta co-stimulatory domains. The anti-CD19 CAR positive viable T cells are expanded and infused back into the patient.

The approval was based on results from the ZUMA-2 trial which showed an objective response rate of 93% in 60 patients with R/R MCL and a median 18-month overall survival rate of 72.9%.


Physicians stay clear of social media

While most physicians (70%) have some kind of social media presence the vast majority are not active, a study of 650 randomly selected doctors at the top 10 US hospitals has found.

Physicians were most likely to have a social media profile on LinkedIn (45%), followed by Facebook (23%) and Twitter 19%) and 7% had a blog or personal webpage.

However, almost 90% had no engagement on social media in recent months in terms of posts or interactions with other users, the survey found.

Physicians had a median of 99 followers on Twitter, 301 on Facebook and 161 followers on LinkedIn. Female physicians were more likely than males to have a social media presence, according to the findings published in JAMA Network Open.

The survey also showed that surgeons had higher number of followers than physicians and were also three times more likely to be active on social media.


Drugs for platelet-mediated thrombosis may be re-targeted for COVID-19 treatment

The inflammation and thrombosis seen in severe COVID-19 disease may be caused by the platelets being activated by anti-SARS-CoV-2 spike protein antibodies, UK researchers say.

A team at Reading University showed that aberrant glycosylation of anti-SARS-CoV-2 IgG immune complexes seen in COVID-19 poatients increased platelet thrombus formation on von Willebrand Factor in vitro.

They also found that activation was dependent on FcγRIIA and showed it was possible to reduce or stop pathogenic platelet activation with therapeutic small molecules R406 (fostamatinib) and ibrutinib, which that inhibit tyrosine kinases Syk and Btk respectively, or by the P2Y12 antagonist cangrelor.

A trial led by Imperial College London and Imperial College Healthcare NHS Trust — called MATIS — is now testing these drugs in clinical trials with patients at hospital sites across the UK to see whether they will reduce serious clotting for hospitalised COVID-19 patients.

Co-investigator Dr Nichola Cooper, consultant haematologist at Imperial College Healthcare NHS Trust, said research around blood clotting related to inflammation had suggested that the drugs already used for other disorders could be easily accessible treatments for COVID-19.

“We are yet to see results from the MATIS trial so we do not yet know how these drugs will work in patients, but our hope is that we can both inhibit the inflammatory response and prevent severe disease and blood clots. It is exciting to see our collaboration with Reading backing our theory already and providing a solid scientific basis for clinical trials.”

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