Table 3.

Mechanism of action and the rate of yearly NEDA with high-efficacy DMTs

Drug	Mechanism of action	Rate of NEDA	Ref
Alemtuzumab	A humanised monoclonal antibody selectively targeting CD52 highly expressed on T and B lymphocytes	58.2a–62.4b % at 5 years	[35, 36]
Natalizumab	α4 integrin antagonist, a selective adhesion molecule inhibitor	27c–40d % at 2 years	[37]
Ocrelizumab	A humanised anti-CD20 antibody	48% at 96 weeks	[38]
Cladribine	A synthetic deoxyadenosine analogue which induces a preferential and sustained reduction in numbers of circulating peripheral T and B lymphocytes	47e % at 96 weeks	[39]

These are yearly NEDA rate and likely to be significantly higher than cumulative NEDA rate over 5 years

^aPatients were treated with DMT prior to participating in the trail

^bPatients were treatment naïve before receiving Alemtuzumab

^cPatients had non-highly active disease, which was defined as fewer than two relapses or no gadolinium-enhancing lesions at study entry

^dPatients had highly active disease, which was defined as at least two relapses in the year before study entry and at least one gadolinium-enhancing lesion at study entry

^ePatients were treated with 3.5 or 5.25 mg/kg of Cladribine