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Posted On: 11/01/2021 4:12:44 PM
Post# of 148878
Brought it over for you. Sometimes things disappear on YMB.
Bridge18 minutes ago
Recknor’s been saying interesting things in recent ccs. This is October 13.
20:30
CR
Sure. It’s important that we make sure that we follow these extension patients. Some of these patients are close to 7 years have been on monotherapy, which is incredible. There’s 3 trials, CD01, CD02, which was the drug resistance, and then CD03. All of these have extended and we’ve got a lot of data on patients that we’re looking at to give us clues about how leronlimab is working and how it’s beneficial.
There is a Mechanism of Action when we first started with this drug that is simply binding to CCR5 as an umbrella to prevent the virus from entering cells. But what we’ve discovered is that that binding actually is an immunomodulator. And it’s fascinating because CCR5, which is what we bind to, is the actual transmission system of our immune system.
And some peoples’ immune systems, from what we’re seeing, don’t work quite right. I think as a physician clinically treating patients, I wasn’t aware of some of these problems that patients were having may actually be due to abnormal immunomodulation, and that’s [inaudible]
Leronlimab binding to this, we’re able to see that in some patients that have the transmission stuck in first or second gear, and move to fifth or sixth gear, that totally changes what the immune system is able to do. And we see really a lot of that has to do with leakiness of vessels. I won’t get too technical.
But It’s very exciting what we’re seeing with NASH.
And we think that that same Mechanism of Action likely is what’s applying to some of the defect in long-haulers, but a host of other indications including stroke, where we’re seeing paresthesias and stroke fatigue get better, to perhaps implications with this particular immunomodulatory defect with diabetic patients, for example. Why some may have worse cases than others. There’s a whole lot of research.
NP
You are working with a laboratory yourself directly now that is testing leronlimab for many different biomarkers that I’m very excited for the -- everyone to know about as soon as you give us the green light to talk about it.
CR
Biomarker was one of the first initiatives. By doing the biomarkers, that helps us be able to select which patients we think would respond. Part of that is also understanding the Mechanism of Action. And knowing all of that helps us better design clinical trials. So our upcoming long-haulers trial, we spent a lot of time into that, a lot of the development actually happened through the biomarker lab.
And what we’re seeing actually in NASH as well.
And we’re just started with the biomarkers, so I look forward to a lot of trials that we can actually accelerate faster by identifying those patients that we can help them better with, that have that predisposition.
SK
Yeah, and Nader, Chris brings up a very good point here, and I think it’s something I want everybody to understand. I mean, originally I got involved in the molecule because I wanted to see -- it never made sense to me why you would wait for a virus to infect the cell and start making billions of copies rather than block it in the outset, right? Why wouldn’t you ever protect healthy cells from viral entry?
But Chris brought up something very important: immunomodulation and NASH, and whether you pick your target of PR [?] or FXR or GLP or galectin proteins. This is different. This is about CCR5 and immunomodulation. We know that CCR5 is present on hepatocytes. We know that CCR5 is present on stellate cells. Stellate cells are what produce the scar tissue in the liver. So this is really a unique approach in NASH that we think has a high likelihood of success based on immunomodulation.
But the same process applies to cancer. It’s about controlling the the tumor microenvironment and immunomodulation.
That’s what’s unique about leronlimab. We started with one thing, we just wanted to protect healthy cells from viral entry, and now we’re finding a whole new aspect of different therapeutic indications.
Bridge18 minutes ago
Recknor’s been saying interesting things in recent ccs. This is October 13.
20:30
CR
Sure. It’s important that we make sure that we follow these extension patients. Some of these patients are close to 7 years have been on monotherapy, which is incredible. There’s 3 trials, CD01, CD02, which was the drug resistance, and then CD03. All of these have extended and we’ve got a lot of data on patients that we’re looking at to give us clues about how leronlimab is working and how it’s beneficial.
There is a Mechanism of Action when we first started with this drug that is simply binding to CCR5 as an umbrella to prevent the virus from entering cells. But what we’ve discovered is that that binding actually is an immunomodulator. And it’s fascinating because CCR5, which is what we bind to, is the actual transmission system of our immune system.
And some peoples’ immune systems, from what we’re seeing, don’t work quite right. I think as a physician clinically treating patients, I wasn’t aware of some of these problems that patients were having may actually be due to abnormal immunomodulation, and that’s [inaudible]
Leronlimab binding to this, we’re able to see that in some patients that have the transmission stuck in first or second gear, and move to fifth or sixth gear, that totally changes what the immune system is able to do. And we see really a lot of that has to do with leakiness of vessels. I won’t get too technical.
But It’s very exciting what we’re seeing with NASH.
And we think that that same Mechanism of Action likely is what’s applying to some of the defect in long-haulers, but a host of other indications including stroke, where we’re seeing paresthesias and stroke fatigue get better, to perhaps implications with this particular immunomodulatory defect with diabetic patients, for example. Why some may have worse cases than others. There’s a whole lot of research.
NP
You are working with a laboratory yourself directly now that is testing leronlimab for many different biomarkers that I’m very excited for the -- everyone to know about as soon as you give us the green light to talk about it.
CR
Biomarker was one of the first initiatives. By doing the biomarkers, that helps us be able to select which patients we think would respond. Part of that is also understanding the Mechanism of Action. And knowing all of that helps us better design clinical trials. So our upcoming long-haulers trial, we spent a lot of time into that, a lot of the development actually happened through the biomarker lab.
And what we’re seeing actually in NASH as well.
And we’re just started with the biomarkers, so I look forward to a lot of trials that we can actually accelerate faster by identifying those patients that we can help them better with, that have that predisposition.
SK
Yeah, and Nader, Chris brings up a very good point here, and I think it’s something I want everybody to understand. I mean, originally I got involved in the molecule because I wanted to see -- it never made sense to me why you would wait for a virus to infect the cell and start making billions of copies rather than block it in the outset, right? Why wouldn’t you ever protect healthy cells from viral entry?
But Chris brought up something very important: immunomodulation and NASH, and whether you pick your target of PR [?] or FXR or GLP or galectin proteins. This is different. This is about CCR5 and immunomodulation. We know that CCR5 is present on hepatocytes. We know that CCR5 is present on stellate cells. Stellate cells are what produce the scar tissue in the liver. So this is really a unique approach in NASH that we think has a high likelihood of success based on immunomodulation.
But the same process applies to cancer. It’s about controlling the the tumor microenvironment and immunomodulation.
That’s what’s unique about leronlimab. We started with one thing, we just wanted to protect healthy cells from viral entry, and now we’re finding a whole new aspect of different therapeutic indications.
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