So it goes without saying I am beyond happy and extremely grateful to have at last started on rituximab, one of the most effective (but unlicensed) disease-modifying MS treatments available to date.
On my first visit I met a string of people in for their monthly natalizumab infusions, from a plucky youngster newly diagnosed and quickly started on treatment, to someone there for his 100th dose, 🤔 about 8 years worth. Had to smile and offer congratulations; made me think there should be milestone T-shirts available!
Joking aside it was interesting sharing stories, a good number of folk seemed to have travelled a reasonable distance with a history of failing to be offered suitable treatment elsewhere. Those fortunate enough to be in the catchment area, particularly the young first-timer in the midst of her A levels, are in the very best place.
As for me, a lot of the damage is done. Rituximab won't do much at this late stage, but something has to be better than nothing. I'm happy and honestly feel there is nothing more that can be done other than continue to eat healthily, keep as fit and active as possible and above all stay positive. Suntan and lipstick should cover the rest.
♧♧♧♧♧
Funnily enough, I first came across rituximab (although didn't know it by that name) 30 years ago in 1988, my first year at the Welsh School of Pharmacy in Cardiff. We were learning about an exciting up and coming new type of drug therapy called monoclonal antibodies. What better way to target a recepter (to this day I think of drug receptors as little squares or triangles stuck to a cell surface) than with its cognate antibody. Tag the cell for destruction and let the body's immune system do its job.
One of the first monoclonal antibody (mAb) immunotherapies (derived from mice, no idea how but I remember a diagram of a mouse and a syringe) in development was rituximab targeting the CD20 protein (surface recepter) found on B cells and would be licensed for treating B cell lymphoma in 1997. It was soon discovered (lateral thinking and someone trying it for the first time?) that rituximab was also effective in treating autoimmune diseases and a licence for rheumatoid arthritis duly followed. Not so multiple sclerosis. With the patent due to expire, the drug company (Genentec, now Roche) had a more lucrative idea. Make a few tweeks to develop a humanised younger brother to be named ocrelizumab (mab stands for monoclonal antibody, the zu indicates humanised). Licensed in the US and Europe in 2018 for RRMS and early or 'active' PPMS and marketed as Ocrevus. Why not for SPMS? I've no idea. Meanwhile the guardians of the NHS purse strings, NICE, got busy negotiating a discount. Trump hates it, reckons the US pay the price.
In the meantime, across the channel in Sweden they decided they'd had enough of paying huge sums for less effective treatments and set about prescribing rituximab off-label. By now the patent for the original Rituxan brand had expired and a slightly cheaper biosimilar (generic) was available. Pharmaceutical companies, understandably, hate this.
I guess Sweden offered ocrelizumab, when licensed, for people who qualified but carried on offering rituximab for those who didn't. Quite right too. There are still no licensed treatments for SPMS and that someone should be told their MS isn't bad enough for the most effective drugs (ocrelizumab, alemtuzumab, natalizumab, cladribine) is crazy.
There must be thousands of people in the UK alone with SPMS and no treatment. I can name a fair few in my home town. I wish more neurologists would recognise that all MS worth treating and prescribe effective treatments off-label (cladribine, rituximab) for those not ticking arbitrary boxes.
