Why In News?
VERVE-102 is an experimental, one-time in vivo base-editing gene therapy designed to permanently switch off the PCSK9 gene in the liver, durably lowering disease-driving bad (LDL) cholesterol.
What is VERVE-102?
-
VERVE-102 is an experimental gene-editing medicine designed to permanently switch off PCSK9 in liver cells, reducing LDL-C over the long term.
-
In-vivo Editing: Unlike ex-vivo therapy, the editing machinery is delivered directly into the patient's body, where it edits target cells.
-
Base Editing: It uses an adenine base editor (ABE) to make a targeted DNA base change without creating the conventional double-strand DNA break associated with many CRISPR approaches.
-
Target: PCSK9 regulates LDL-receptor availability in the liver; reducing PCSK9 helps the liver remove more LDL-C from blood.
-
Delivery: VERVE-102 uses a GalNAc-LNP system and is administered through an intravenous infusion targeting liver cells.).
-
Single Course: The objective is to replace repeated cholesterol-lowering treatment with one durable genetic intervention, although long-term durability is still being established.
What is Base Editing?
|
How Does VERVE-102 Work?
-
Step 1: An intravenous infusion introduces VERVE-102 into the bloodstream.
-
Step 2: Its GalNAc-LNP delivery system facilitates uptake into liver cells.
-
Step 3: The LNP releases base-editor mRNA and guide RNA inside the cells.
-
Step 4: Cells translate the mRNA into the adenine base-editing protein.
-
Step 5: The guide RNA directs the editor towards the PCSK9 DNA sequence.
-
Step 6: The editor makes a targeted A-to-G DNA change designed to permanently inactivate PCSK9.
-
Step 7: Reduced PCSK9 activity allows more LDL receptors to remain available on liver cells.
-
Result: Greater LDL clearance from blood can produce a long-lasting reduction in LDL-C.
What is PCSK9?
-
PCSK9 is a protein involved in controlling the number of LDL receptors on liver cells.
-
Normal Function: PCSK9 promotes degradation of LDL receptors, reducing the liver's ability to remove LDL-C.
-
Gene Inactivation: Lowering PCSK9 increases LDL-receptor availability and therefore enhances LDL-C clearance.
-
Therapeutic Logic: Human genetics provides strong evidence that naturally lower PCSK9 activity is associated with lower cardiovascular risk, supporting PCSK9 as a drug target.
What is LDL Cholesterol?
-
LDL-C: Low-density lipoprotein cholesterol transports cholesterol through the bloodstream and is commonly called “bad cholesterol.”
-
Plaque Formation: Persistently elevated LDL-C contributes to cholesterol deposition in arterial walls.
-
Atherosclerosis: Long-term LDL exposure promotes atherosclerotic plaque formation, narrowing arteries and increasing cardiovascular risk.
-
Clinical Link: High LDL-C is an important modifiable risk factor for heart attack and stroke.
Source: INDIANEXPRESS
PRACTICE QUESTIONQ. With reference to VERVE-102, consider the following statements:
Which of the statements given above are correct? A. 1 and 2 only B. 1, 2 and 4 only C. 2 and 3 only D. 1, 2, 3 and 4 Answer: B Explanation: Statement 1 is correct: VERVE-102 targets the PCSK9 gene in the liver to permanently lower LDL cholesterol. Statement 2 is correct: It uses an in-vivo base-editing approach (specifically an adenine base editor) to modify the DNA sequence. Statement 3 is incorrect: VERVE-102 is currently an investigational medicine in clinical trials (e.g., Phase 1b Heart-2 trial) and is not an approved treatment for routine use. Statement 4 is correct: It is delivered using a proprietary liver-directed GalNAc-LNP (lipid nanoparticle) delivery system, which targets the asialoglycoprotein receptor (ASGPR) on liver cells. |