The idea is based on the same basic idea as our previous studies, namely that ME in a subgroup of patients is often a non-infectious disease which comes after some form of trigger in patients who are otherwise previously healthy. And what we think is that the body creates antibodies that we create against everything we have and to defend ourselves against the environment - an antibody that affects the body itself. And it has been shown in recent years that after infections, such as COVID infection or Epstein-Barr virus, mumps virus or other infections, the body creates many antibodies that affect molecules, its own molecules in the body. And some of these we believe are involved in affecting the function of so-called functional autoantibodies and may be involved in disrupting the balance in the body so that patients can get the characteristic symptoms.
Central to this is probably the regulation of blood flow in the tissue in relation to stress. It is certain that when patients are stressed, they quickly develop ME/CFS. They have problems increasing circulation enough, for example with exertion, which causes us to get these characteristic symptoms of fatigue, feeling sick, exertion intolerance, cognitive symptoms, lethargy, and things like that.
So this pilot study is based on influencing the so-called plasma cells, which are cells in the immune system that are primarily responsible for creating antibodies. And we give a medicine called Daratumumab, which is an antibody that is used in cancer treatment for patients who have so-called myelomatosis or bone marrow cancer, because it lowers the level of these plasma cells, also benign plasma cells. So when we use it, the purpose is to temporarily reduce the number of plasma cells in the system and then, as a result, the antibody levels in the blood are temporarily reduced. And then we hope that the effect can be sustained in some patients, so that when those antibodies are reduced, it leads to an improvement in the patients' symptoms.
And what we have seen in the pilot study is that 60% of those, that is, 6 out of 10 patients that we have included, have apparently had a good effect on the symptoms of the disease. And of five of the six patients have experienced a clinical improvement, then the response or improvement has been sustained for up to two years, as long as we have followed the patients. One of the patients had a relatively early relapse after 3 months, a partial relapse, while the other five patients have had a sustained effect.
We haven't had any significant side effects from this. No serious medical events. So we believe that tolerance has been good so far. We have given a little over 50 such injections. And these injections are given subcutaneously, i.e. under the skin of the abdomen. And it has actually worked well. But even though we have seen that it has had a good effect in these patients, we believe that there is reason to do a larger study. And the main reason is that we cannot draw any firm conclusions based on such a small pilot study with 10 patients. We cannot be sure that the medication alone is the cause of the observed improvements.
So that's why we have to do what we call a double-blind study where some of the patients receive active medicine and some of the patients receive inactive injections without active medicine, without either us or the patient knowing what they have received. It is certainly a double-blind and placebo-controlled study. We have planned this and are thinking of starting it, hopefully before or after the summer when the studies have been approved by the authorities.
And initially we are thinking of including 66 patients, where 44 patients will receive active medicine with this Daratumumab medicine that will reduce the number of plasma cells and 22 patients on placebo, i.e. an inactive injection that does not affect the immune system. And then these patients will be followed up for three months after inclusion in the study before they receive the first injection. And then they should be followed for 15 months after they start treatment, so 18 months in total. And when the last patient has been observed for 18 months, the study is closed. And then we will know who has received active treatment and who has received placebo and can compare the results. And then we can get a relatively certain impression of whether this medication is useful for patients, if it is important that it provides good responses that last over time in a sufficiently large proportion of patients.
So we hope that the study can get started and we hope that it can help raise the level of knowledge about the disease and perhaps be a contribution to helping develop rational treatment. But we should not draw any firm conclusions until we have seen the results from the analyzed study, that is, the double-blind study, lest we be mistaken.
We have tried to learn from all the studies we have done before in order to learn in a way to create a good protocol for the study that is now about to start. This means that we have tried to work with the inclusion criteria. We have tried to work out what impact goals we should have for the study. We have incorporated continuous step counting with activity watches throughout the entire study. We have included some tests that they can do without the patients getting too tired. And we have a number of questionnaires that the patient must fill out regularly throughout the study - validated forms that report symptom burden to try to find out whether this has a beneficial effect or not.
When it comes to the number of patients we plan to include, it is clear that we have worked in collaboration with statisticians and so on with how many patients we need to be able to show whether there is a difference between the active group and the placebo group. And it is clear that when we only really have our own data from previous studies to build on and observations from this pilot study that we have talked about, that estimate is a bit uncertain because the number of patients that is necessary to show depends on how big the difference is between the patients on average in relation to the placebo group on average, and we must be open to saying that we have tried to estimate this as best as we can.
But the number of patients that can be included is also limited by the economy because this is an expensive biomedicine. The drug company that sells this didn't want to give any discount for the research study. And it is difficult to get public funding. We've seen it here and there, so what is there is that the patients and the patient association and private individuals so far make it possible to do this study. And we are very grateful for that. And we must then try as best we can to create the best possible protocol, make the best possible assessment of how the study will be conducted so that we manage this money as well as possible.
We cannot promise that such a study will be positive, but we can try to do our best. And the underlying calculations suggest that if what we have seen in the pilot studies is fairly representative, then we should have a chance of showing a definite difference. And then we have estimated that there should be no more than 20% responses as stated in the placebo group. And compared to previous studies, we have tightened the response requirements significantly. There are much stricter requirements to meet response criteria in this study than before. And that's because of what we've learned.
We have also done a study where we have only followed patients over time without giving them treatment to try to find out what the normal variation is for different patients over time. What we want to try to avoid is to avoid what are normal symptom changes interfering with the criteria for response so that we try to separate true responses caused by drug treatment from natural variation. And then we see that we should not include patients who have the mildest degree of illness. Not because it can't be bothersome enough for the patients, but because they fluctuate too much after we include them that we are afraid that we can increase the so-called response rate in placebo.
If we don't get this study done, probably no one else will. We have been at it for a long time and we believe that we have come across a principle and a mechanism that is important to explain. And it's clear that our immune system is extremely complex and difficult and extensive. And there are many different things that influence each other. Nevertheless, when we try to say that we are reducing the plasma cells when it will reduce the antibodies that will provide improvement, there is a basic idea about how we will affect the immune system. But it is clear that we are always aware that it is much more complex than that. But it looks like that intervention is doing something beneficial for patient outcomes. As I say, it is based on two years of observation of these patients and with a backdrop of experiences from previous studies.
