M. Noureddin1, E. Lawitz 2, A. Ritter3, T. Hassane
Post# of 148154
(Total Views: 760)
Posted On: 04/05/2024 11:33:21 PM
M. Noureddin1, E. Lawitz 2, A. Ritter3, T. Hassanein4, K. Bowman5, J. Sacha6, E. Mahyari6, S. Hansen6, S. Kelly7, and C. Recknor7 1Houston Liver Institute, Houston, TX, USA. 2Texas Liver Institute, University of Texas Health San Antonio, San Antonio, TX, USA. 3Center for Advanced Research & Education, Gainesville, GA, USA. 4Southern California GI & Liver Centers, CA, USA. 5Sensible Healthcare Clinical Research, Ocoee, FL, USA. 6OHSU, Portland, OR, USA. 7CytoDyn Inc. Vancouver, WA, USA
BACKGROUND
NONALCOHOLIC STEATOHEPATITIS
• Non-alcoholic steatohepatitis (NASH) is a chronic liver disease characterized by the presence of hepatic inflammation and cell injury due to hepatic fat
accumulation (steatosis) in ≥ 5% of hepatocytes.
• Patients with advanced fibrosis due to NASH are at significantly higher risk of liver‐related mortality.
• Despite its very high burden, there are currently no approved pharmacological therapies for NASH.
• Recent studies targeting chemokine-mediated inflammatory signalling pathways that may reduce liver fat and scar tissue formation indicate the great potential of immune modulation as a therapeutic strategy in NASH (1).
CCR5 AND THE INFLAMMATORY RESPONSE
• In NASH, liver homeostasis is impaired due to an accumulation of toxic lipids which can activate both Kupffer cells (KCs) and tissue-resident macrophages
resulting in the production of fibrogenic cytokines and chemoattractant chemokines such as transforming growth factor-beta (TGF-
and monocyte
chemoattractant protein-1 (MCP-1).
• Not only do these cytokines/chemokines promote transdifferentiation of hepatic stellate cells (HSCs) into myofibroblasts (primary source for fibrillary collagens),
but they also amplify the immune response by recruiting additional cells into the damaged area.
• Recruitment of extra-hepatic inflammatory cells to the site of hepatic injury is typically mediated by interactions between cytokines/chemokines and their
receptors.
• It has also been shown that patients with NASH also have high levels of C-C chemokine receptor 5 (CCR5) and the associated ligand, CCL5, thus demonstrating a potential role of CCR5 and its ligands in liver fibrosis.
• Furthermore, anti-inflammatory and anti-fibrotic effects have been reported in pre-clinical models of NASH following the use of monoclonal antibodies targeting chemokine signalling pathways (3).
• CCR5 has thus become an attractive target for the clinical development of new antifibrotic therapies (2).
PRECLINICAL DATA: LERONLIMAB AND CCR5
• Leronlimab (PRO 140) is a humanized IgG4,κ monoclonal antibody (mAb) to the C-C chemokine receptor type 5 (CCR5), under development as a therapy for Human Immunodeficiency Virus (HIV) infection and other indications.
• The potential for leronlimab in the treatment of NASH was demonstrated in a pre-clinical model of fatty liver disease. Immunodeficient, NOD-SCID Gamma (NSG)
mice were fed a high fat, NASH-inducing diet, transplanted with human stem cells to repopulate the deficient immune system, and treated with leronlimab.
• 16 male NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ, commonly known as the NOD scid IL-2 receptor gamma knockout mice (NSG) were first humanized by intravenous inoculation with normal human umbilical cord blood cells (105). After 5 weeks on normal mouse chow, mice were successfully humanized, demonstrating > 25% human CD45 cells in peripheral blood. Mice were switched to high fat (52%) high cholesterol (1.25%) diet (FPC diet: fructose, palmitate, cholesterol, trans-fat; Envigo-Teklad TD.160785). Leronlimab and control antibody (normal human IgG, Sigma) were administered i.p. at a dose of 2 mg i.p. twice weekly, n=8 mice/group. Mice were euthanized at 16 weeks after initiation of FPC diet.
• The results showed that leronlimab inhibited fatty liver development, a key characteristic of early-stage NASH (manuscript in press; see below)
A. Fatty deposits in NSG mice fed High Fat, High Cholesterol diet. Images show frozen section stained with Oil Red O were scanned at 20X and digitized using Aperio AT2 slide scanner (Leica Biosystems, and analyzed using QuPath v0.2.01 imaging software). B. Comparison of Hepatic Steatosis in leronlimab vs.
IgG-treated NSG mice fed a high fat, high cholesterol diet.
Graph shows mean Oil red O positive pixels, relative to entire region of interest (ROI) and standard error (SE) were calculated for both treatment groups. Percent positivity in IgG treated group was 9.751 ± 1.789. Percent positivity in leronlimab treated group was 3.207 ±1.515. Student’s t test p=0.014. Steatosis was numerically scored following semi-quantitative pathological standard.
(....That's page #1...i'll paste 2 pages per Post because i don't know the text limit here. The link won't copy, & hope my spacing is ok from cell phone, after hit Post....)
Page 2:
AIM
REFERENCES
1. Lefere S, Puengel T, Hundertmark J, Penners C, Frank AK, Guillot A, de Muynck K, Heymann F, Adarbes V,
Defrêne E, Estivalet C, Geerts A, Devisscher L, Wettstein G, Tacke F. Differential effects of selective- and pan-PPAR agonists on experimental steatohepatitis and hepatic macrophages. J Hepatol. 2020 Oct;73(4):757-770. doi: 10.1016/j.jhep.2020.04.025. Epub 2020 Apr 29. PMID: 32360434. 2. Lefebvre E, M. G. Antifibrotic Effects of the Dual CCR2/CCR5 Antagonist Cenicriviroc in Animal Models of Liver and Kidney Fibrosis. 2016; 11(6), e0158156.
METHOD
Subjects who meet all eligibility criteria, as per data gathered from the screening period qualify for
enrollment. All subjects who fail to meet eligibility criteria will be considered screen failure and exit
the study without further evaluation. The study consisted of two parts:
• Part 1 of the study, eligible subjects randomized to 1:1 to one of the two study arms to receive
leronlimab 700 mg (Group A), or placebo (Group given once per week (±1 day) at the study
site for up to 13 weeks during the treatment period (with up to 60 participants).
• Leronlimab 700 mg SC weekly injection (Group A)
• Placebo SC weekly injection (Group
• Part 2 of the study, eligible subjects enrolled to receive leronlimab 350 mg open label given
one per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up
to 28 participants).
• Leronlimab 350 mg SC weekly injection
Primary efficacy objective:
Change from baseline in hepatic fat fraction, assessed by magnetic resonance imaging-derived
proton density fat fraction (MRI-PDFF) at week 14.
Secondary efficacy objective:
Change from baseline in fibro-inflammatory activity in the liver as assessed by cT1 (corrected T1)
at week 14. cT1 is obtained by multiparametric magnetic resonance imaging of the liver and is a
quantitative metric for assessing a composite of liver inflammation and fibrosis, expressed in
milliseconds (msec). Additional objectives were change from baseline in LFT, chemokine and
cytokine levels and key biomarkers of inflammation to week 14.
A. Fatty deposits in NSG mice fed High Fat, High Cholesterol diet. Images show frozen section stained with Oil Red O were scanned at 20X and digitized using Aperio AT2 slide scanner (Leica Biosystems, and analyzed using QuPath v0.2.01 imaging software). B. Comparison of Hepatic Steatosis in leronlimab vs.
IgG-treated NSG mice fed a high fat, high cholesterol diet.
Graph shows mean Oil red O positive pixels, relative to entire region of interest (ROI) and standard error (SE) were calculated for both treatment groups. Percent positivity in IgG treated group was 9.751 ± 1.789. Percent positivity in leronlimab treated group
was 3.207 ±1.515. Student’s t test p=0.014. Steatosis was numerically scored following semi-quantitative pathological standard.
A. B.
• All analyses performed were exploratory.
• Treatment with leronlimab was generally well tolerated in both Part 1 and Part 2.
Part 1
• Leronlimab 700 mg did not reduce mean change in PDFF and cT1 from baseline to week 14 vs.
placebo.
Part 2
• Leronlimab 350 mg significantly reduced mean change in PDFF and cT1 from baseline to week
14 vs. placebo.
• Despite increased fibro-inflammation, in patients with moderate and severe cT1 values at baseline, leronlimab 350 mg still showed significantly reduced cT1 from baseline to week 14 vs. placebo.
Part 1 & Part 2 pooled
• Pooled 350 mg + 700 mg group also had significant reductions in PDFF and cT1 vs. placebo.
• Although small sample size (n=5) CCR5 haplotype analysis is suggestive that specific-haplotypes may be better suited for the 700 mg dose of leronlimab.
• The CCR5 promoter region has been shown to play a critical role in CCR5 transcriptional regulation of disease progression for HIV, HBV, Chagas, heart disease and cancer.
• CCR5 transcriptional activity, disease progression can be slowed or accelerated.
• Based on these data, we hypothesized that not only does surface CCR5 expression level
likely play a part in NASH disease progression, but CCR5 specific haplotypes would correlate with dose and treatment outcomes.
• Serum analysis
• Reductions in ALT, AST and Alkaline Phosphatase were observed in the 350 mg group
and cT1 subgroups vs placebo with corresponding reductions in VCAM, CCL2, CCL3, CCL5, CCL18, INF gamma, IL-6, IL-8, IL-1 Receptor Antagonist (IL-1RA), TNF Receptor 2, Tissue Inhibitor of MMP-1 and EN RAGE.
• The mechanism of action for leronlimab appears to be multifactorial involving VCAM, CCL2, CCL3, CCL11, and CCL18 in addition to competitive binding of CCR5 effecting metabolic and fibro-inflammatory parameters.
• The mechanism of action for leronlimab appears to be multifactorial involving VCAM, CCL2, CCL3, CCL11, and CCL18 in addition to competitive binding of CCR5 effecting metabolic and fibro-inflammatory parameters.
Protocol:
Adverse Events (Safety):
Serum Chemistry and Labs:
Demographics:
CDI-NASH-01 was designed as a multi-center Phase 2a trial and was subsequently converted into an exploratory study to evaluate dose, efficacy, and safety of leronlimab 700 mg and 350 mg along with biomarkers to help design future trials and
understand potential mechanisms of action of leronlimab.
Primary Objective of the Part 1 study was to assess the efficacy of leronlimab 700 mg (n=22) in improving NAFLD/NASH tests in adult patients diagnosed with NASH compared to placebo (n=28).
Part 2 was subsequently added to assess 350
mg in improving NAFLD/NASH tests in adult patients diagnosed with NASH (n=22).
Secondary Objective of this study was to assess the safety and tolerability of leronlimab in adult patients diagnosed with NASH compared to placebo.
Eligibility: Eligible patients included adults aged between 18 to 75 years (inclusive), with evidence of phenotype nonalcoholic steatohepatitis (NASH). Patients had a Body Mass Index (BMI) ≥ 28 kg/m2 and were required to demonstrate the presence of hepatic fat fraction, as defined by ≥ 8% on MRI-PDFF and cT1 ≥ 800 milliseconds (msec) at screening. A stable body weight (±5%) was required during the 6 months prior to screening. Exclusion criteria include but were not limited to HIV, autoimmune hepatitis, excess alcohol use, viral hepatitis, and prior or pending liver transplantation, refer to www.clinicaltrials.gov for further exclusion criteria.
METHOD
Subjects who meet all eligibility criteria, as per data gathered from the screening period qualify for
enrollment. All subjects who fail to meet eligibility criteria will be considered screen failure and exit
the study without further evaluation. The study consisted of two parts:
• Part 1 of the study, eligible subjects randomized to 1:1 to one of the two study arms to receive
leronlimab 700 mg (Group A), or placebo (Group given once per week (±1 day) at the study
site for up to 13 weeks during the treatment period (with up to 60 participants).
• Leronlimab 700 mg SC weekly injection (Group A)
• Placebo SC weekly injection (Group
• Part 2 of the study, eligible subjects enrolled to receive leronlimab 350 mg open label given
one per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up
to 28 participants).
• Leronlimab 350 mg SC weekly injection
Primary efficacy objective:
Change from baseline in hepatic fat fraction, assessed by magnetic resonance imaging-derived proton density fat fraction (MRI-PDFF) at week 14.
Secondary efficacy objective:
Change from baseline in fibro-inflammatory activity in the liver as assessed by cT1 (corrected T1)
at week 14. cT1 is obtained by multiparametric magnetic resonance imaging of the liver and is a
quantitative metric for assessing a composite of liver inflammation and fibrosis, expressed in milliseconds (msec). Additional objectives were change from baseline in LFT, chemokine and cytokine levels and key biomarkers of inflammation to week 14
_______
I like this section:
" Part 2
• Leronlimab 350 mg significantly reduced mean change in PDFF and cT1 from baseline to week
14 vs. placebo.
BACKGROUND
NONALCOHOLIC STEATOHEPATITIS
• Non-alcoholic steatohepatitis (NASH) is a chronic liver disease characterized by the presence of hepatic inflammation and cell injury due to hepatic fat
accumulation (steatosis) in ≥ 5% of hepatocytes.
• Patients with advanced fibrosis due to NASH are at significantly higher risk of liver‐related mortality.
• Despite its very high burden, there are currently no approved pharmacological therapies for NASH.
• Recent studies targeting chemokine-mediated inflammatory signalling pathways that may reduce liver fat and scar tissue formation indicate the great potential of immune modulation as a therapeutic strategy in NASH (1).
CCR5 AND THE INFLAMMATORY RESPONSE
• In NASH, liver homeostasis is impaired due to an accumulation of toxic lipids which can activate both Kupffer cells (KCs) and tissue-resident macrophages
resulting in the production of fibrogenic cytokines and chemoattractant chemokines such as transforming growth factor-beta (TGF-
and monocyte chemoattractant protein-1 (MCP-1).
• Not only do these cytokines/chemokines promote transdifferentiation of hepatic stellate cells (HSCs) into myofibroblasts (primary source for fibrillary collagens),
but they also amplify the immune response by recruiting additional cells into the damaged area.
• Recruitment of extra-hepatic inflammatory cells to the site of hepatic injury is typically mediated by interactions between cytokines/chemokines and their
receptors.
• It has also been shown that patients with NASH also have high levels of C-C chemokine receptor 5 (CCR5) and the associated ligand, CCL5, thus demonstrating a potential role of CCR5 and its ligands in liver fibrosis.
• Furthermore, anti-inflammatory and anti-fibrotic effects have been reported in pre-clinical models of NASH following the use of monoclonal antibodies targeting chemokine signalling pathways (3).
• CCR5 has thus become an attractive target for the clinical development of new antifibrotic therapies (2).
PRECLINICAL DATA: LERONLIMAB AND CCR5
• Leronlimab (PRO 140) is a humanized IgG4,κ monoclonal antibody (mAb) to the C-C chemokine receptor type 5 (CCR5), under development as a therapy for Human Immunodeficiency Virus (HIV) infection and other indications.
• The potential for leronlimab in the treatment of NASH was demonstrated in a pre-clinical model of fatty liver disease. Immunodeficient, NOD-SCID Gamma (NSG)
mice were fed a high fat, NASH-inducing diet, transplanted with human stem cells to repopulate the deficient immune system, and treated with leronlimab.
• 16 male NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ, commonly known as the NOD scid IL-2 receptor gamma knockout mice (NSG) were first humanized by intravenous inoculation with normal human umbilical cord blood cells (105). After 5 weeks on normal mouse chow, mice were successfully humanized, demonstrating > 25% human CD45 cells in peripheral blood. Mice were switched to high fat (52%) high cholesterol (1.25%) diet (FPC diet: fructose, palmitate, cholesterol, trans-fat; Envigo-Teklad TD.160785). Leronlimab and control antibody (normal human IgG, Sigma) were administered i.p. at a dose of 2 mg i.p. twice weekly, n=8 mice/group. Mice were euthanized at 16 weeks after initiation of FPC diet.
• The results showed that leronlimab inhibited fatty liver development, a key characteristic of early-stage NASH (manuscript in press; see below)
A. Fatty deposits in NSG mice fed High Fat, High Cholesterol diet. Images show frozen section stained with Oil Red O were scanned at 20X and digitized using Aperio AT2 slide scanner (Leica Biosystems, and analyzed using QuPath v0.2.01 imaging software). B. Comparison of Hepatic Steatosis in leronlimab vs.
IgG-treated NSG mice fed a high fat, high cholesterol diet.
Graph shows mean Oil red O positive pixels, relative to entire region of interest (ROI) and standard error (SE) were calculated for both treatment groups. Percent positivity in IgG treated group was 9.751 ± 1.789. Percent positivity in leronlimab treated group was 3.207 ±1.515. Student’s t test p=0.014. Steatosis was numerically scored following semi-quantitative pathological standard.
(....That's page #1...i'll paste 2 pages per Post because i don't know the text limit here. The link won't copy, & hope my spacing is ok from cell phone, after hit Post....)
Page 2:
AIM
REFERENCES
1. Lefere S, Puengel T, Hundertmark J, Penners C, Frank AK, Guillot A, de Muynck K, Heymann F, Adarbes V,
Defrêne E, Estivalet C, Geerts A, Devisscher L, Wettstein G, Tacke F. Differential effects of selective- and pan-PPAR agonists on experimental steatohepatitis and hepatic macrophages. J Hepatol. 2020 Oct;73(4):757-770. doi: 10.1016/j.jhep.2020.04.025. Epub 2020 Apr 29. PMID: 32360434. 2. Lefebvre E, M. G. Antifibrotic Effects of the Dual CCR2/CCR5 Antagonist Cenicriviroc in Animal Models of Liver and Kidney Fibrosis. 2016; 11(6), e0158156.
METHOD
Subjects who meet all eligibility criteria, as per data gathered from the screening period qualify for
enrollment. All subjects who fail to meet eligibility criteria will be considered screen failure and exit
the study without further evaluation. The study consisted of two parts:
• Part 1 of the study, eligible subjects randomized to 1:1 to one of the two study arms to receive
leronlimab 700 mg (Group A), or placebo (Group
given once per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up to 60 participants).
• Leronlimab 700 mg SC weekly injection (Group A)
• Placebo SC weekly injection (Group
• Part 2 of the study, eligible subjects enrolled to receive leronlimab 350 mg open label given
one per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up
to 28 participants).
• Leronlimab 350 mg SC weekly injection
Primary efficacy objective:
Change from baseline in hepatic fat fraction, assessed by magnetic resonance imaging-derived
proton density fat fraction (MRI-PDFF) at week 14.
Secondary efficacy objective:
Change from baseline in fibro-inflammatory activity in the liver as assessed by cT1 (corrected T1)
at week 14. cT1 is obtained by multiparametric magnetic resonance imaging of the liver and is a
quantitative metric for assessing a composite of liver inflammation and fibrosis, expressed in
milliseconds (msec). Additional objectives were change from baseline in LFT, chemokine and
cytokine levels and key biomarkers of inflammation to week 14.
A. Fatty deposits in NSG mice fed High Fat, High Cholesterol diet. Images show frozen section stained with Oil Red O were scanned at 20X and digitized using Aperio AT2 slide scanner (Leica Biosystems, and analyzed using QuPath v0.2.01 imaging software). B. Comparison of Hepatic Steatosis in leronlimab vs.
IgG-treated NSG mice fed a high fat, high cholesterol diet.
Graph shows mean Oil red O positive pixels, relative to entire region of interest (ROI) and standard error (SE) were calculated for both treatment groups. Percent positivity in IgG treated group was 9.751 ± 1.789. Percent positivity in leronlimab treated group
was 3.207 ±1.515. Student’s t test p=0.014. Steatosis was numerically scored following semi-quantitative pathological standard.
A. B.
• All analyses performed were exploratory.
• Treatment with leronlimab was generally well tolerated in both Part 1 and Part 2.
Part 1
• Leronlimab 700 mg did not reduce mean change in PDFF and cT1 from baseline to week 14 vs.
placebo.
Part 2
• Leronlimab 350 mg significantly reduced mean change in PDFF and cT1 from baseline to week
14 vs. placebo.
• Despite increased fibro-inflammation, in patients with moderate and severe cT1 values at baseline, leronlimab 350 mg still showed significantly reduced cT1 from baseline to week 14 vs. placebo.
Part 1 & Part 2 pooled
• Pooled 350 mg + 700 mg group also had significant reductions in PDFF and cT1 vs. placebo.
• Although small sample size (n=5) CCR5 haplotype analysis is suggestive that specific-haplotypes may be better suited for the 700 mg dose of leronlimab.
• The CCR5 promoter region has been shown to play a critical role in CCR5 transcriptional regulation of disease progression for HIV, HBV, Chagas, heart disease and cancer.
• CCR5 transcriptional activity, disease progression can be slowed or accelerated.
• Based on these data, we hypothesized that not only does surface CCR5 expression level
likely play a part in NASH disease progression, but CCR5 specific haplotypes would correlate with dose and treatment outcomes.
• Serum analysis
• Reductions in ALT, AST and Alkaline Phosphatase were observed in the 350 mg group
and cT1 subgroups vs placebo with corresponding reductions in VCAM, CCL2, CCL3, CCL5, CCL18, INF gamma, IL-6, IL-8, IL-1 Receptor Antagonist (IL-1RA), TNF Receptor 2, Tissue Inhibitor of MMP-1 and EN RAGE.
• The mechanism of action for leronlimab appears to be multifactorial involving VCAM, CCL2, CCL3, CCL11, and CCL18 in addition to competitive binding of CCR5 effecting metabolic and fibro-inflammatory parameters.
• The mechanism of action for leronlimab appears to be multifactorial involving VCAM, CCL2, CCL3, CCL11, and CCL18 in addition to competitive binding of CCR5 effecting metabolic and fibro-inflammatory parameters.
Protocol:
Adverse Events (Safety):
Serum Chemistry and Labs:
Demographics:
CDI-NASH-01 was designed as a multi-center Phase 2a trial and was subsequently converted into an exploratory study to evaluate dose, efficacy, and safety of leronlimab 700 mg and 350 mg along with biomarkers to help design future trials and
understand potential mechanisms of action of leronlimab.
Primary Objective of the Part 1 study was to assess the efficacy of leronlimab 700 mg (n=22) in improving NAFLD/NASH tests in adult patients diagnosed with NASH compared to placebo (n=28).
Part 2 was subsequently added to assess 350
mg in improving NAFLD/NASH tests in adult patients diagnosed with NASH (n=22).
Secondary Objective of this study was to assess the safety and tolerability of leronlimab in adult patients diagnosed with NASH compared to placebo.
Eligibility: Eligible patients included adults aged between 18 to 75 years (inclusive), with evidence of phenotype nonalcoholic steatohepatitis (NASH). Patients had a Body Mass Index (BMI) ≥ 28 kg/m2 and were required to demonstrate the presence of hepatic fat fraction, as defined by ≥ 8% on MRI-PDFF and cT1 ≥ 800 milliseconds (msec) at screening. A stable body weight (±5%) was required during the 6 months prior to screening. Exclusion criteria include but were not limited to HIV, autoimmune hepatitis, excess alcohol use, viral hepatitis, and prior or pending liver transplantation, refer to www.clinicaltrials.gov for further exclusion criteria.
METHOD
Subjects who meet all eligibility criteria, as per data gathered from the screening period qualify for
enrollment. All subjects who fail to meet eligibility criteria will be considered screen failure and exit
the study without further evaluation. The study consisted of two parts:
• Part 1 of the study, eligible subjects randomized to 1:1 to one of the two study arms to receive
leronlimab 700 mg (Group A), or placebo (Group
given once per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up to 60 participants).
• Leronlimab 700 mg SC weekly injection (Group A)
• Placebo SC weekly injection (Group
• Part 2 of the study, eligible subjects enrolled to receive leronlimab 350 mg open label given
one per week (±1 day) at the study site for up to 13 weeks during the treatment period (with up
to 28 participants).
• Leronlimab 350 mg SC weekly injection
Primary efficacy objective:
Change from baseline in hepatic fat fraction, assessed by magnetic resonance imaging-derived proton density fat fraction (MRI-PDFF) at week 14.
Secondary efficacy objective:
Change from baseline in fibro-inflammatory activity in the liver as assessed by cT1 (corrected T1)
at week 14. cT1 is obtained by multiparametric magnetic resonance imaging of the liver and is a
quantitative metric for assessing a composite of liver inflammation and fibrosis, expressed in milliseconds (msec). Additional objectives were change from baseline in LFT, chemokine and cytokine levels and key biomarkers of inflammation to week 14
_______
I like this section:
" Part 2
• Leronlimab 350 mg significantly reduced mean change in PDFF and cT1 from baseline to week
14 vs. placebo.
(7)
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