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RecruitingNCT07428473STX-1150-01Updated Sep 21, 2026

A Study of STX-1150 in Participants With Elevated Low-Density Lipoprotein Cholesterol (LDL-C)

A Phase 1 interventional study of STX-1150 in Elevated LDL-C and High Cholesterol, sponsored by Monash University. Recruiting at 3 sites in 2 countries. Open to participants aged 18 Years to 70 Years. Per ClinicalTrials.gov, last updated 2026-09-21.

Sponsored by Monash University · Phase 1, Interventional, and Treatment

Phase
Phase 1
Study type
Interventional
Enrollment
64
Allocation
Not applicable
Ages
18 Years to 70 Years
Sex
All
01

Study summary

STX-1150 is an investigational therapy designed to lower LDL-C by silencing a gene called PCSK9 in the liver. STX-1150 does not edit or permanently change the gene. STX-1150 comprises an mRNA and guide RNA (gRNA) delivered via lipid nanoparticles (LNP) for intravenous infusion. The mRNA produces a protein that switches off the PCSK9 gene expression without altering the DNA sequence. This process leverages natural mechanisms that regulate gene activity.

The study will enroll up to 64 participants with elevated LDL-C across sites in Australia and New Zealand. The follow-up period will be up to 1- year post-treatment.

Read the detailed description

STX-1150 is an investigational product designed to epigenetically silence the PCSK9 gene. It comprises an mRNA and a guide RNA (gRNA) delivered in a lipid nanoparticle (LNP) for intravenous (IV) infusion.

STX-1150 epigenetically silences the expression of the PCSK9 gene in the liver, thereby reducing circulating PCSK9 and LDL-C levels. The active components, an mRNA and a gRNA are encapsulated in lipid nanoparticles (LNPs) for targeted hepatic delivery. The gRNA precisely guides the complex to a specific locus within the PCSK9 gene promoter.

By reducing PCSK9 expression, STX-1150 prevents the degradation of LDL receptors (LDL-R), leading to increased LDL-R levels on hepatocytes and enhanced clearance of LDL-C from the bloodstream. This targeted and durable epigenetic silencing represents a promising therapeutic strategy for long-term LDL-C reduction, particularly benefiting patients with elevated LDL-C or a high risk for Atherosclerotic Cardiovascular Disease (ASCVD).

02

Conditions studied

  • Elevated LDL-C and High Cholesterol

Keywords

  • LDL-C
  • PCSK9
  • Cardiovascular Disease
  • ASCVD
  • CMD
  • Genomic medicine
  • Gene Therapy
  • Atherosclerosis
  • Cholesterol
  • Heart Attack
  • Hypertension
  • Hypercholesterolemia
  • CVM
  • Cardiometabolic Disease
  • Epigenetic
  • CRISPR
03

Who can participate

Ages eligible
18 Years to 70 Years
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  • Elevated serum LDL-C with or without LDL-C lowering medication
  • Willing and able to give informed consent before initiation of any study-related procedures and willing to comply with all required study procedures

Exclusion criteria

Exclusion Criteria:

  • Patients with history of an ASCVD event \</= 6 months.
  • Any uncontrolled or serious disease, or any medical or surgical condition that may interfere with participation
  • Diagnosis of familial hypercholesterolemia
  • Active or history of liver disease
  • Previous treatment with PCSK9-inhibitor or other prior treatment within a specified timeframe
  • Clinically significant abnormal laboratory values
04

Study design

Phase
Phase 1
Primary purpose
Treatment
Allocation
Not applicable
Intervention model
Single group
Masking
None (open label)
Enrollment
64 participants (estimated)

Study arms

  • Experimental
    Arm 1

    Part 1: An open-label, single ascending dose will serve to identify the Dose-Limiting Toxicities (DLTs) and Optimal Biological Dose (OBD) of STX-1150. Part 2: Following Part 1, an open-label, single or multi-dose expansion of the OBD cohort will be conducted to further characterize the effect of STX-1150 and obtain additional safety data at the OBD.

    Drug: STX-1150

Interventions

  • DrugSTX-1150

    Drug: STX-1150 is an investigational product designed to epigenetically silence the PCSK9 gene. Epigenome modulation offers a way to silence genes without changing their underlying DNA sequence.

05

What researchers measure

Primary outcomes

  1. Incidence and Severity of Treatment-Emergent Adverse Events (TEAEs)

    Time frame: Up to Week 52 from administration of STX-1150

  2. Incidence and Severity of Serious Adverse Events (SAEs)

    Time frame: Up to Week 52 from administration of STX-1150

  3. Incidence and Severity of Adverse Events of Special Interest (AESI)

    Time frame: Up to Week 52 from administration of STX-1150

Secondary outcomes

  1. Incidence of dose-limiting toxicities (DLTs)

    Time frame: Within 14 days from administration of STX-1150

  2. Percent Change from Baseline in Plasma PCSK9 Concentration

    Time frame: Up to Week 52

  3. Percent Change from Baseline in LDL-C

    Time frame: Up to 52 weeks

  4. Plasma Concentrations of STX-1150 Lipid Components

    Time frame: Up to 52 weeks

  5. Number of Participants with Treatment-Induced Immunogenicity

    Time frame: Up to 52 Weeks

  6. Absolute Change from Baseline in LDL-C

    Time frame: Up to 52 weeks

  7. The Absolute Change from Baseline in Plasma PCSK9 Concentration

    Time frame: Up to Week 52

06

Study locations

3 of 3 sites recruiting
  • Monash Health/ Victorian Heart Hospital (VHH)
    Clayton, Victoria 3168, Australia
    Recruiting
  • Aotearoa Clinical Trials/Middlemore Hospital
    Papatoetoe, Auckland 2025, New Zealand
    Recruiting
  • New Zealand Clinical Research (NZCR)
    Christchurch, Christchurch 8011, New Zealand
    Recruiting
07

Registry details

Key details

Study ID
NCT07428473
Lead sponsor
Monash University
Collaborators
Scribe Therapeutics Inc.
Responsible party
Stephen Nicholls (Program Medical Director, Victorian Heart Hospital, Monash University) — Principal investigator
First posted
Feb 23, 2026
Start date
Jun 30, 2026
Primary completion
Dec 30, 2028 (estimated)
Completion
Dec 30, 2028 (estimated)
Last update
Sep 21, 2026

Study contacts

Domenic Sacca
Contact
domenic.sacca@monash.edu
+61 423245187
Raeda Mustafa
Contact
raeda.mustafa@monash.edu
+61 477581540
Stephen Nicholls, MBBS, FRACP, PhD
study chair · VHI

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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