While the study directly compared Calcitriol + D3 againt methylprednisolone and found it was far superior in terms of remission and the ability to remain relapse free, the study also looked at the literature for Tysabri, Interferon beta, and glatiramer acetate and shows how marked superior calcitriol + D3 is against all these standard DMDs.
Although this is a study in EAE mice which as we know is not MS, it is a comparison against how these drugs performed in EAE mice.
I would say there is considerable urgency to get this tested in humans because even if it only matches the performance of these drugs, it would mean savings of billions of dollars.
"Thus, in this direct comparison, only the calcitriol/+D treatment induced lasting remissions in all animals and significantly reversed EAE disability. We conclude that the calcitriol/+D protocol is markedly more effective than IFNβ, mAb to α4β1I, or GLAT in the rodent MS model."
I compiled this table comparing the drugs against Calcitriol + D3 from the data in the study. The table does not appear in the study.
Source URL: http://www.ncbi.nlm.nih.gov/pubmed/23968560
Journal Title: Journal of neuroimmunology
Journal Date: 6 Aug 2013
Abstract URL: http://www.ncbi.nlm.nih.gov/pubmed/2396 ... t=abstract
Article Title: One calcitriol dose transiently increases Helios(+)FoxP3(+) T cells and ameliorates autoimmune demyelinating disease.
Article Authors: Faye E Nashold,Corwin D Nelson,Lauren M Brown,Colleen E Hayes
Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706, United States.
Here is the relevant quote from the study:
3.6. Efficacy of the calcitriol/+D protocol compared to other MS treatments
It is instructive to compare the calcitriol/+D protocol with published EAE treatment data for three approved MS drugs, IFNβ (Yu et al., 1996), monoclonal antibodies to alpha4 integrin (mAb to α4I) (Kent et al., 1995), and GLAT (Teitelbaum et al., 1999). Data from these studies were compared to the data shown in Fig. 5A, expressing the disability scores as percentages of the maximum score to facilitate direct comparisons. As detailed above, the calcitriol/+D protocol, when administered to animals with partial to complete paralysis of both hind limbs, halted disease progression in all animals, gradually reduced the mean EAE disability score by 61% (from 2.3 to 0.9), and completely prevented relapses over a 60 day observation period (Fig. 5A and Suppl. Fig. 2A). For comparison, alternate day IFNβ treatments administered to animalswith first EAE signs (loss of tail tone) reduced the mean EAE disability score 14% (from 3.5 to 3.0), and reduced relapses/mouse from 2.2 to 1.2 over a 56 day observation period (Yu et al., 1996) (Suppl. Fig. 2B). Administering mAb to α4I to animals with first EAE signs and again 3 days later transiently reduced the EAE
Administering mAb to α4I [Tysabri] to animals with first EAE signs and again 3 days later transiently reduced the EAE disability score by 20%, before disease progression resumed and disability of the treated animals approached the placebo animals over a 42 day observation period (Kent et al., 1995) (Suppl. Fig. 2C). Alternate day GLAT treatments beginning one week before EAE disease induction delayed disease onset slightly but did not inhibit disease progression although the treatments decreased the final EAE disability score ~45% relative to the placebo group at the end of a 25 day observation period (Teitelbaum et al., 1999) (Suppl. Fig. 2D). Thus, in this direct comparison, only the calcitriol/+D treatment induced lasting remissions in all animals and significantly reversed EAE disability. We conclude that the calcitriol/+D protocol is markedly more effective than IFNβ mAb to α4β1I, or GLAT in the rodent MS model.