scholarly journals TNF-α inhibitors used as steroid-sparing maintenance monotherapy in parenchymal CNS sarcoidosis

2021 ◽  
pp. jnnp-2020-325665
Author(s):  
Frédéric Hilezian ◽  
Adil Maarouf ◽  
Clemence Boutiere ◽  
Audrey Rico ◽  
Sarah Demortiere ◽  
...  
Keyword(s):  
Primary Outcome ◽  
Immunosuppressive Agents ◽  
Minimum Dose ◽  
Tnf Α ◽  
The Mean ◽  
Factor Α ◽  
Necrosis Factor ◽  
Steroid Sparing

ObjectiveTo assess the efficacy of tumour necrosis factor-α (TNF-α) inhibitors used as steroid-sparing monotherapy in central nervous system (CNS) parenchymal sarcoidosis.MethodsThe French Multiple Sclerosis and Neuroinflammation Centers retrospectively identified patients with definite or probable CNS sarcoidosis treated with TNF-α inhibitors as steroid-sparing monotherapy. Only patients with CNS parenchymal involvement demonstrated by MRI and imaging follow-up were included. The primary outcome was the minimum dose of steroids reached that was not associated with clinical or imaging worsening during a minimum of 3 months after dosing change.ResultsOf the identified 38 patients with CNS sarcoidosis treated with TNF-α inhibitors, 23 fulfilled all criteria (13 females). Treatments were infliximab (n=22) or adalimumab (n=1) for a median (IQR) of 24 (17–40) months. At treatment initiation, the mean (SD) age was 41.5 (10.5) years and median (IQR) disease duration 22 (14–49.5) months. Overall, 60% of patients received other immunosuppressive agents before a TNF-α inhibitor. The mean (SD) minimum dose of steroids was 31.5 (33) mg before TNF-α inhibitor initiation and 6.5 (5.5) mg after (p=0.001). In all, 65% of patients achieved steroids dosing <6 mg/day; 61% showed clinical improvement, 30% stability and 9% disease worsening. Imaging revealed improvement in 74% of patients and stability in 26%.ConclusionTNF-α inhibitors can greatly reduce steroids dosing in patients with CNS parenchymal sarcoidosis, even refractory.Classification of evidenceThis study provides Class IV evidence that TNF-α inhibitor used as steroid-sparing monotherapy is effective for patients with CNS parenchymal sarcoidosis.

scholarly journals Infliximab for the treatment of CNS sarcoidosis

Neurology ◽  
2017 ◽  
Vol 89 (20) ◽  
pp. 2092-2100 ◽  
Author(s):  
Jeffrey M. Gelfand ◽  
Michael J. Bradshaw ◽  
Barney J. Stern ◽  
David B. Clifford ◽  
Yunxia Wang ◽  
...  
Keyword(s):  
Neurologic Recovery ◽  
Clinical Responses ◽  
The Mean ◽  
Treatment Responses ◽  
Factor Α ◽  
Lost To Follow Up ◽  
Necrosis Factor ◽  
Clinical Stability

Objective:To describe clinical and imaging responses in neurosarcoidosis to infliximab, a monoclonal antibody against tumor necrosis factor–α.Methods:Investigators at 6 US centers retrospectively identified patients with CNS sarcoidosis treated with infliximab, including only patients with definite or probable neurosarcoidosis following rigorous exclusion of other causes.Results:Of 66 patients with CNS sarcoidosis (27 definite, 39 probable) treated with infliximab for a median of 1.5 years, the mean age was 47.5 years at infliximab initiation (SD 11.7, range 24–71 years); 56.1% were female; 62.1% were white, 37.0% African American, and 3% Hispanic. Sarcoidosis was isolated to the CNS in 19.7%. Using infliximab doses ranging from 3 to 7 mg/kg every 4–8 weeks, MRI evidence of a favorable treatment response was observed in 82.1% of patients with imaging follow-up (n = 56), with complete remission of active disease in 51.8% and partial MRI improvement in 30.1%; MRI worsened in 1 patient (1.8%). There was clinical improvement in 77.3% of patients, with complete neurologic recovery in 28.8%, partial improvement in 48.5%, clinical stability in 18.2%, worsening in 3%, and 1 lost to follow-up. In 16 patients in remission when infliximab was discontinued, the disease recurred in 9 (56%), typically in the same neuroanatomic location.Conclusions:Most patients with CNS sarcoidosis treated with infliximab exhibit favorable imaging and clinical treatment responses, including some previously refractory to other immunosuppressive treatments.Classification of evidence:This study provides Class IV evidence that for patients with CNS sarcoidosis infliximab is associated with favorable imaging and clinical responses.

scholarly journals The clinical significance of tumor necrosis factor-α plasma level in patients having chronic lymphocytic leukemia

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1215-1219 ◽  
Author(s):  
Alessandra Ferrajoli ◽  
Michael J. Keating ◽  
Taghi Manshouri ◽  
Francis J. Giles ◽  
Amanda Dey ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Lymphocytic Leukemia ◽  
Tnf Α ◽  
The Mean ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α), a cytokine possessing pleiotropic biological activities, is produced by leukemic lymphocytes in patients with chronic lymphocytic leukemia (CLL) and acts as an autocrine and paracrine growth factor in this disease. In this study, TNF-α levels were determined in 150 patients with CLL and correlated with disease characteristics, prognostic factors, and survival. The mean TNF-α plasma concentration in the patients with CLL was significantly higher than in the healthy control population (16.4 versus 8.7 pg/mL; P &lt; .0001). Patients having an elevated TNF-α level had more advanced Rai and Binet stage disease, higher serum β2-microglobulin (β2M) levels, a greater percentage of cells expressing CD38, and lower hemoglobin and platelet levels. Patients having chromosomal abnormalities such as 11q deletion, trisomy 12, and chromosome 17 aberrations had a higher mean TNF-α level (27.5 pg/mL) than patients having a diploid karyotype or other miscellaneous cytogenetic abnormalities (14.2 pg/mL;P &lt; .001). The TNF-α level was a predictor of survival when the Cox proportional hazards model was used with TNF-α entered as a continuous variable (P = .0001). Also, patients having a TNF-α level above the mean value of 14 pg/mL had significantly shorter survival duration (P = .00001). The TNF-α level remained predictive of survival in Cox multivariate analysis independent of Rai staging and β2M, hemoglobin, prior therapy, white cell count, and platelet level (P = .005). We conclude that the TNF-α level serves as a prognostic factor in patients with CLL and that inhibition of TNF-α in these patients could have therapeutic importance.

scholarly journals ASSOCIATION OF TUMOR NECROSIS FACTOR-α–238G>A AND APOLIPOPROTEIN E2 POLYMORPHISMS WITH INTRACRANIAL HEMORRHAGE AFTER BRAIN ARTERIOVENOUS MALFORMATION TREATMENT

Neurosurgery ◽  
2007 ◽  
Vol 61 (4) ◽  
pp. 731-740 ◽  
Author(s):  
Achal S. Achrol ◽  
Helen Kim ◽  
Ludmila Pawlikowska ◽  
K. Y. Trudy Poon ◽  
Charles E. McCulloch ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Arteriovenous Malformation ◽  
Arteriovenous Malformations ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Brain Arteriovenous Malformation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract OBJECTIVE We previously reported specific genotypes of polymorphisms in two genes, tumor necrosis factor-α (TNF-α-238G &gt; A) and Apolipoprotein E (ApoE e2), as independent predictors of new intracranial hemorrhage (ICH) in the natural course of untreated brain arteriovenous malformations. We hypothesized that the risk of posttreatment ICH would also be greater in patients with brain arteriovenous malformations with these genotypes. METHODS Two hundred fifteen patients undergoing brain arteriovenous malformation treatment (embolization, arteriovenous malformation resection, radiosurgery, or any combination of these) were genotyped and followed longitudinally. Association of genotype with new symptomatic ICH after initiation of treatment was assessed using Cox proportional hazards adjusted for treatment type, demographics, and established ICH risk factors censored at the time of the last follow-up evaluation or death. RESULTS The cohort was 48% male and 55% Caucasian, and 52% had an ICH before the initiation of treatment; the mean age ± standard deviation was 36.6 ± 17.2 years. Posttreatment ICH occurred in 34 (16%) patients with a median follow-up period of 1.9 years (interquartile range, 1.6 yr). After adjustment, the risk of posttreatment ICH was greater for TNF-α-238 AG genotype (hazard ratio [HR], 3.5; 95% confidence interval [CI], 1.3–9.8; P = 0.016) and ApoE e2 (HR, 3.2; 95% CI, 1.0–9.7; P = 0.042). Similar trends for the TNF-α-238 AG genotype were seen in surgery (HR, 4.2; 95% CI, 0.6–28.8; P = 0.14) and radiosurgery subsets (HR, 3.8; 95% CI, 0.7–19.4; P = 0.11). An effect of ApoE e2 was seen in radiosurgery subsets (HR, 10.9; 95% CI, 1.3–93.7; P = 0.030), but not in surgery subsets (HR, 1.4; 95% CI, 0.3–7.4; P = 0.67). CONCLUSION Despite a variety of different mechanisms for posttreatment hemorrhage, these data suggest that the TNF-α and ApoE genotypes may contribute common phenotypes of enhanced vascular instability that increase the risk of hemorrhagic outcome.

scholarly journals Common Variations in the Genes Encoding C-Reactive Protein, Tumor Necrosis Factor-α, and Interleukin-6, and the Risk of Clinical Diabetes in the Women's Health Initiative Observational Study

2011 ◽  
Vol 57 (2) ◽  
pp. 317-325 ◽  
Author(s):  
Kei-hang K Chan ◽  
Kathleen Brennan ◽  
Nai-chieh Y You ◽  
Xuyang Lu ◽  
Yiqing Song ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Genes Encoding ◽  
Factor Α ◽  
Necrosis Factor

BACKGROUND Circulating concentrations of high-sensitivity C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) have been associated with an increased risk of diabetes. METHODS To examine the roles of genetic variation in the genes encoding CRP, TNF- α, and IL-6 in the development of diabetes, we conducted a prospective case–control study nested within the Women's Health Initiative Observational Study. We followed 82 069 postmenopausal women (50–79 years of age) with no history of diabetes for incident diabetes for a mean follow-up of 5.5 years. We identified 1584 cases and matched them with 2198 controls with respect to age, ethnicity, clinical center, time of blood draw, and length of follow-up. We genotyped 13 haplotype-tagging single-nucleotide polymorphisms (tSNPs) across 2.3 kb of the CRP (C-reactive protein, pentraxin-related) gene, 16 tSNPs across 2.8 kb of the TNF (tumor necrosis factor) gene, and 14 tSNPs across 4.8 kb of the IL6 [interleukin 6 (interferon, beta 2)] gene. Plasma concentrations of TNF-α receptor 2 (TNF-α-R2) and IL-6 were measured. RESULTS After adjusting for matching factors, confounding variables, and multiple comparisons, we found 8 variants in the TNF gene to be associated with plasma TNF-α-R2 concentrations in white women (q &lt; 0.05). After adjusting for multiple comparisons (q &gt; 0.05), we found no association of any IL6 gene variant with plasma IL-6 concentration, nor did we find any significant associations between any SNPs among these 3 genes and diabetes risk (q &gt; 0.05). CONCLUSIONS We found modest associations between TNF variants and circulating concentrations of TNF-α-R2. Common variants of the CRP, TNF, and IL6 genes were not significantly associated with risk of clinical diabetes in postmenopausal women.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals POS0204 AUTOANTIBODIES AND SYSTEMIC LUPUS ERYTHEMATOSUS INDUCED BY ANTI-TUMOUR NECROSIS FACTOR ALPHA THERAPY IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 318.1-318
Author(s):  
D. Santos Oliveira ◽  
A. Martins ◽  
F. R. Martins ◽  
F. Oliveira Pinheiro ◽  
M. Rato ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Disease Duration ◽  
Seroconversion Rate ◽  
Necrosis Factor Alpha ◽  
Malar Rash ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Over Time

Background:Anti-tumour necrosis factor alpha (anti-TNF-α) therapy is commonly used to treat inflammatory conditions such as rheumatoid arthritis (RA). Autoantibodies namely antinuclear antibodies (ANA) induced by these treatments are well established. However, anti-TNF-α-induced systemic lupus erythematosus (SLE) is rarely described and its incidence is yet unknown.Objectives:This study aimed to determine the prevalence of ANA seroconversion and to characterize the development of SLE induced by anti-TNF-α therapy in patients with RA over time.Methods:An observational retrospective cohort study was conducted with at least one year of follow-up. Patients with diagnosis of RA, according to American College of Rheumatology criteria (ACR), and registered on Rheumatic Diseases Portuguese Register (Reuma.pt) who started their first anti-TNFα between 2003 and 2019 were included. Patients with positive ANA (titer ≥100) and/or positive double-strand DNA (dsDNA) antibodies and/or with a diagnosis of SLE at their first visit were excluded. Demographic, clinical and laboratory data were obtained by consulting Reuma.pt. As there are no recognized criteria for drug-induced SLE, the diagnosis of SLE induced by anti-TNF-α was considered if there is a temporal relationship between clinical manifestations and anti-TNF-α-therapy, the presence of at least 1 serologic ACR criteria (ANA or anti-dsDNA) and at least 1 nonserologic ACR criteria (arthritis, serositis, hematologic disorder or malar rash) [1]. Continuous variables are presented with mean, standard deviation, median, quartile 1 and quartile 3. Categorical variables are presented with absolute and relative frequencies.Results:A total of 211 patients (mean age of 49.9±10.9 years old; 84.4% female) were included with a median follow-up time of 6 [3-14] years. We found a seroconversion rate for ANA of 75.4% (n=159) with median treatment duration of 31 [8.5-70.5] months. The most common titre was 1/100 with diffuse and speckled patterns. ANA seroconversion was higher for etanercept (47.8%, n=76) than with adalimumab (23.9%, n=38), infliximab (13.8%, n=22), golimumab (12.6%, n=20) or certolizumab (1.9%, n=3). SLE induced by anti-TNF-α occurred in two patients (0.9%) with erosive and seropositive (rheumatoid factor and anti-citrullinated protein antibodies) RA previously treated with two conventional synthetic disease-modifying antirheumatic drugs, including methotrexate. The first patient, a female with 66 years old and 17 years of disease duration, developed SLE after 16 months of infliximab, with constitutional symptoms, abrupt worsening of polyarthritis, ANA titer of 1/320 diffuse pattern and positive dsDNA (248 UI/mL) antibodies. The second patient, a woman with 43 years old and 11 years of disease duration, developed SLE after 41 months of adalimumab with malar rash and ANA titer of 1/320 diffuse pattern, positive dsDNA (285 UI/mL), positive anti-histone antibodies and hypocomplementemia. In these two cases, anti-TNF-α therapy was stopped and recovery was spontaneous without treatment. The first patient switched to adalimumab and the second switched to golimumab without recurrence of SLE for more than ten years.Conclusion:We found a high rate of ANA seroconversion induced by anti-TNFα therapy in patients with RA. However, similar to previous literature, only 0.9% of patients developed SLE with mild manifestations without major organ involvement. Although the drug with the highest ANA seroconversion rate was etanercept, those responsible for induced SLE were infliximab and adalimumab. Patients improved after discontinuation of therapy and tolerated an alternative anti-TNF-α drug without recurrence of induced SLE over time. Therefore, ANA and SLE induced by anti-TNF-α should be considered and reported in the follow-up of RA patients. Further research is needed to explore the impact of this adverse event on the outcomes of treatment over time.References:[1]Hochberg MC. Arthritis Rheum. 1997;40(9):1725.Disclosure of Interests:None declared

scholarly journals Impact of comprehensive management on clinical outcomes in hypertensive patients with coronary artery disease: HIJ-CREATE sub-study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Ogawa ◽  
H Sekiguchi ◽  
K Jujo ◽  
E Kawada-Watanabe ◽  
H Arashi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Primary Outcome ◽  
Ldl Cholesterol ◽  
Lipid Lowering ◽  
Hypertensive Patients ◽  
Mean Values ◽  
Comprehensive Management ◽  
The Mean ◽  
Artery Disease

Abstract Background There are limited data on the effects of blood pressure (BP) control and lipid lowering in secondary prevention of coronary artery disease (CAD) patients. We report a secondary analysis of the effects of BP control and lipid management in participants of the HIJ-CREATE, a prospective randomized trial. Methods HIJ-CREATE was a multicenter, prospective, randomized, controlled trial that compared the effects of candesartan-based therapy with those of non-ARB-based standard therapy on major adverse cardiac events (MACE; a composite of cardiovascular death, non-fatal myocardial infarction, unstable angina, heart failure, stroke, and other cardiovascular events requiring hospitalization) in 2,049 hypertensive patients with angiographically documented CAD. In both groups, titration of antihypertensive agents was performed to reach the target BP of &lt;130/85 mmHg. The primary endpoint was the time to first MACE. Incidence of endpoint events in addition to biochemistry tests and office BP was determined during the scheduled 6, 12, 24, 36, 48, and 60-month visits. Achieved systolic BP and LDL-Cholesterol (LDL-C) level were defined as the mean values of these measurements in patients who did not develop MACEs and as the mean values of them prior to MACEs in those who developed MACEs during follow-up. Results During a median follow-up of 4.2 years (follow-up rate of 99.6%), the primary outcome occurred in 304 patients (30.3%). Among HIJ-CREATE participants, 905 (44.2%) were prescribed statins on enrollment. Kaplan–Meier curves for the primary outcome revealed that there was no relationship between statin therapy and MACEs in hypertensive patients with CAD. The original HIJ-CREATE population was divided into 9 groups based on equal tertiles based on mean achieved BP and LDL-C during follow-up. For the analysis of subgroups, estimates of relative risk and the associated 95% CIs were generated with a Cox proportional-hazards model (Figure 1). The relation between LDL cholesterol level and hazard ratios for MACEs was nonlinear, with a significant increase of MACEs only in the patients with inadequate controlled LDL-C level even in the patients with tightly controlled BP. Conclusions The results of the post-hoc analysis of the HIJ-CREATE suggest that clinicians should pay careful attention to conduct comprehensive management of lipid lowering even in the contemporary BP lowering for the secondary prevention in hypertensive patients with CAD. Figure 1 Funding Acknowledgement Type of funding source: None

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

scholarly journals Real-World Clinical Outcomes Associated with Canagliflozin in Patients with Type 2 Diabetes Mellitus in Spain: The Real-Wecan Study

2020 ◽  
Vol 9 (7) ◽  
pp. 2275
Author(s):  
Juan J. Gorgojo-Martínez ◽  
Manuel A. Gargallo-Fernández ◽  
Alba Galdón Sanz-Pastor ◽  
Teresa Antón-Bravo ◽  
Miguel Brito-Sanfiel ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Real World ◽  
Primary Outcome ◽  
Baseline Hba1c ◽  
Real World Setting ◽  
Antihyperglycemic Therapy ◽  
The Mean ◽  
Hba1c Levels

The aims of this multicentric retrospective study were to assess in a real-world setting the effectiveness and safety of canagliflozin 100 mg/d (CANA100) as an add-on to the background antihyperglycemic therapy, and to evaluate the intensification of prior sodium–glucose co-transporter type 2 inhibitor (SGLT-2i) therapy by switching to canagliflozin 300 mg/d (CANA300) in patients with T2DM. One cohort of SGLT2i-naïve patients with T2DM who were initiated on CANA100 and a second cohort of patients with prior background SGLT-2i therapy who switched to CANA300 were included in the study. The primary outcome of the study was the mean change in HbA1c over the follow-up time. In total, 583 patients were included—279 in the cohort of CANA100 (HbA1c 8.05%, weight 94.9 kg) and 304 in the cohort of CANA300 (HbA1c 7.51%, weight 92.0 kg). Median follow-up periods in both cohorts were 9.1 and 15.4 months respectively. CANA100 was associated to significant reductions in HbA1c (−0.90%) and weight (−4.1 kg) at the end of the follow-up. In those patients with baseline HbA1c > 8% (mean 9.25%), CANA100 lowered HbA1c levels by 1.51%. In the second cohort, patients switching to CANA300 experienced a significant decrease in HbA1c (−0.35%) and weight (−2.1 kg). In those patients with baseline HbA1c > 8% (mean 8.94%), CANA300 lowered HbA1c levels by 1.12%. There were significant improvements in blood pressure in both cohorts. No unexpected adverse events were reported. In summary, CANA100 (as an add-on therapy) and CANA300 (switching from prior SGLT-2i therapy) significantly improved several cardiometabolic parameters in patients with T2DM.

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