Bioventix plc

(“Bioventix” or “the Company”)

Director Dealing

Bioventix plc (BVXP), a UK company specialising in the development and commercial supply of high-affinity monoclonal antibodies for applications in clinical diagnostics, announces that on 29 April 2024 Bruce Hiscock, Chief Financial Officer of the Company, purchased a total of 11 ordinary shares of 5 pence each in the Company (“Ordinary Shares”), at an average price of 4,452 pence per Ordinary Share (the “Purchase”). The Ordinary Shares were purchased under a dividend reinvestment plan (“DRIP”).

Following the Purchase, Bruce Hiscock has a beneficial interest in 789 Ordinary Shares, representing approximately 0.01 per cent. of the issued share capital of the Company.

The notification below, made in accordance with the requirements of the EU Market Abuse Regulation, provides further details.

For further information please contact:

Notification and public disclosure of transactions by persons discharging managerial responsibilities and persons closely associated with them

TR-1: Notification of major interest in shares. To download this report as a PDF file click here.

Abstract

Objectives
To investigate whether circulating acute-phase brain-derived tau (BD-tau) is associated with functional outcome after ischemic stroke.

Methods
Plasma tau was measured by a novel assay that selectively quantifies BD-tau in the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), which includes adult cases with ischemic stroke and controls younger than 70 years, and in an independent cohort of adult cases of all ages (SAHLSIS2). Associations with unfavorable 3-month functional outcome (modified Rankin scale score >2) were analyzed by logistic regression. Various stratified and sensitivity analyses were performed, for example, by age, stroke severity, recanalization therapy, and etiologic subtype.

Results
This study included 454 and 364 cases from the SAHLSIS and SAHLSIS2, with a median age of 58 and 68 years, respectively. Higher acute BD-tau concentrations were significantly associated with increased odds of unfavorable outcome after adjustment for age, sex, day of blood draw, and stroke severity (NIH stroke scale score) in both cohorts (OR per doubling of BD-tau: 2.9 [95% CI 2.2–3.7], P = 1 × 10−15 and 1.8 [1.5–2.2], P = 7 × 10−9, respectively). The association was consistent in the different stratified and sensitivity analyses.

Discussion
BD-tau is a promising blood-based biomarker of ischemic stroke outcomes, and future studies in larger cohorts are warranted.

Interim Report and Financial Statements for the 6 months to 31 December 2023

To download this report as a PDF file click here.

Abstract

Staging amyloid-beta (Aβ) pathophysiology according to the intensity of neurodegeneration could identify individuals at risk for cognitive decline in Alzheimer’s disease (AD). In blood, phosphorylated tau (p-tau) associates with Aβ pathophysiology but an AD-type neurodegeneration biomarker has been lacking. In this multicenter study (n = 1076), we show that brain-derived tau (BD-tau) in blood increases according to concomitant Aβ (“A”) and neurodegeneration (“N”) abnormalities (determined using cerebrospinal fluid biomarkers); We used blood-based A/N biomarkers to profile the participants in this study; individuals with blood-based p-tau+/BD-tau+ profiles had the fastest cognitive decline and atrophy rates, irrespective of the baseline cognitive status. Furthermore, BD-tau showed no or much weaker correlations with age, renal function, other comorbidities/risk factors and self-identified race/ethnicity, compared with other blood biomarkers. Here we show that blood-based BD-tau is a biomarker for identifying Aβ-positive individuals at risk of short-term cognitive decline and atrophy, with implications for clinical trials and implementation of anti-Aβ therapies.

Abstract

Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer’s disease (AD) neuropathologic change and clinical stage. Certain plasma p-tau217 assays recognize tau forms phosphorylated additionally at threonine-212, but the contribution of p-tau212 alone to AD is unknown. We developed a blood-based immunoassay that is specific to p-tau212 without cross-reactivity to p-tau217. Here, we examined the diagnostic utility of plasma p-tau212. In five cohorts (n = 388 participants), plasma p-tau212 showed high performances for AD diagnosis and for the detection of both amyloid and tau pathology, including at autopsy as well as in memory clinic populations. The diagnostic accuracy and fold changes of plasma p-tau212 were similar to those for p-tau217 but higher than p-tau181 and p-tau231. Immunofluorescent staining of brain tissue slices showed prominent p-tau212 reactivity in neurofibrillary tangles that co-localized with p-tau217 and p-tau202/205. These findings support plasma p-tau212 as a peripherally accessible biomarker of AD pathophysiology.