SFA Therapeutics 發表關於治療乙型肝炎和慢性肝病的新方法的研

StephenW

SFA Therapeutics 發表關於治療乙型肝炎和慢性肝病的新方法的研究
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SFA Therapeutics, Inc.
格林威治標準時間 2022 年 9 月 23 日 12:00
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一種治療乙型肝炎和慢性肝病的新方法，目標是開發一種功能性治愈方法
抑制乙型肝炎病毒的藥物都不能治愈。 SFA Therapeutics 的研究表明，靶向病毒編碼蛋白 HBx 可以減少病毒複製和慢性肝病。”
— 馬克·費特爾森博士

美國賓夕法尼亞州詹金敦，2022 年 9 月 23 日/EINPresswire.com/ -- SFA Therapeutics, Inc. 很高興地宣布我們在乙型肝炎研究的新出版物，我們正在開發一種有可能成為功能性治愈。

根據賓夕法尼亞州費城坦普爾大學生物學教授 Mark Feitelson 博士的說法，“全世界有超過 2.5 億乙型肝炎攜帶者面臨發展為慢性肝病及其進展為肝細胞癌的風險。儘管有有許多抑制乙型肝炎病毒複製的藥物，但沒有一種是治愈性的。SFA Therapeutics 的研究現在強調，靶向病毒編碼蛋白 HBx 將減少病毒複製和慢性肝病。與其他治療方式相結合，很可能這一添加將使我們更接近於乙型肝炎的功能性治愈。”

乙型肝炎病毒 (HBV) 攜帶者患慢性肝病 (CLD) 的風險很高，該疾病從肝炎發展為纖維化、肝硬化和肝細胞癌 (HCC)。乙型肝炎編碼的 X 抗原 HBx 促進病毒基因表達和復制，保護受感染的肝細胞免受免疫破壞，並促進 CLD 和 HCC 的發展。對於病毒複製，HBx 調節共價閉合環狀 (ccc) HBV DNA 轉錄，而對於 CLD，HBx 部分通過觸發刺激先天免疫的線粒體損傷觸發細胞氧化應激。 HBx 對 NF-κB 的組成型激活通過轉錄激活促炎基因，導致肝細胞破壞、再生和 HBx 基因與宿主基因組的整合增加。 NF-κB 還具有保肝作用，可維持受感染細胞的存活。多種治療方法包括直接作用的抗病毒化合物和免疫刺激藥物，但未能實現功能性治愈，部分原因是尚未設計出針對 HBx 的治療方法。此外，許多肝硬化或 HCC 患者幾乎沒有或沒有病毒複製，但仍繼續從整合模板中表達 HBx，這表明 HBx 有助於 CLD 的發病機制。因此，阻斷 HBx 活動將影響與實現功能性治愈相關的宿主-病毒關係的多個方面。

HBx 表達和功能的治療性抑制可能有助於在肝硬化和 HCC 發展之前進行功能性治愈。 SFA Therapeutics, Inc. 幫助贊助了這項研究，並正在努力幫助開發基於這些發現的治療方法。根據這項研究，已授予兩項美國專利。

愛爾蘭共和軍
SFA Therapeutics, Inc.
+1 267-584-1080
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StephenW

SFA Therapeutics Publishes Research on its New Approach to Treating Hepatitis B and Chronic Liver Disease
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SFA Therapeutics, Inc.
September 23, 2022, 12:00 GMT
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A new approach to treating Hepatitis B and Chronic Liver Disease, with the the goal of developing a functional cure
None of the drugs that suppress hepatitis B virus are curative. SFA Therapeutics' research shows that targeting virus encoded protein HBx diminishes both virus replication and chronic liver disease.”
— Dr. Mark Feitelson

JENKINTOWN, PA, UNITED STATES, September 23, 2022 /EINPresswire.com/ -- SFA Therapeutics, Inc. is pleased to announce a new publication of our research in hepatitis B, where we are developing a drug that has the potential to become a functional cure.

According to Mark Feitelson, PhD, Professor of Biology at Temple University in Philadelphia, PA, "there are more than 250 million carriers of hepatitis B worldwide who are at risk for the development of chronic liver disease and its progression to hepatocellular carcinoma. Although there are many drugs that suppress hepatitis B virus replication, none are curative. Research from SFA Therapeutics has now highlighted that targeting the virus encoded protein, HBx, will diminish both virus replication and chronic liver disease. In combination with other treatment modalities, it is likely that this addition will bring us closer to a functional cure for hepatitis B."

Patients who are carriers of the hepatitis B virus (HBV) are at high risk of chronic liver disease (CLD) which proceeds from hepatitis, to fibrosis, cirrhosis and to hepatocellular carcinoma (HCC). The hepatitis B-encoded X antigen, HBx, promotes virus gene expression and replication, protects infected hepatocytes from immunological destruction, and promotes the development of CLD and HCC. For virus replication, HBx regulates covalently closed circular (ccc) HBV DNA transcription, while for CLD, HBx triggers cellular oxidative stress, in part, by triggering mitochondrial damage that stimulates innate immunity. Constitutive activation of NF-κB by HBx transcriptionally activates pro-inflammatory genes, resulting in hepatocellular destruction, regeneration, and increased integration of the HBx gene into the host genome. NF-κB is also hepatoprotective, which sustains the survival of infected cells. Multiple therapeutic approaches include direct-acting anti-viral compounds and immune-stimulating drugs, but functional cures were not achieved, in part, because none were yet devised to target HBx. In addition, many patients with cirrhosis or HCC have little or no virus replication, but continue to express HBx from integrated templates, suggesting that HBx contributes to the pathogenesis of CLD. Blocking HBx activity will, therefore, impact multiple aspects of the host–virus relationship that are relevant to achieving a functional cure.

Therapeutic inhibition of HBx expression and function could contribute to a functional cure prior to the development of cirrhosis and HCC. SFA Therapeutics, Inc. has helped sponsor this research, and is working to help develop therapeutics based on these findings. Two US patents have been granted based upon this research.

Ira Spector
SFA Therapeutics, Inc.
+1 267-584-1080
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