Ignite Creation Date:
2024-05-06 @ 3:31 PM
Last Modification Date:
2024-10-26 @ 1:50 PM
Study NCT ID:
NCT04651634
Status:
RECRUITING
Last Update Posted:
2023-04-24
First Post:
2020-11-26
Brief Title:
MIT-001 for Prevention of CCRT-Induced OM in HNSCC Patients
Sponsor:
MitoImmune Therapeutics
Organization:
MitoImmune Therapeutics
Study Overview
Official Title:
A Phase 2 Randomized Double-Blind Placebo Controlled Trial to Evaluate the Safety and Efficacy of MIT-001 in Prevention of Oral Mucositis in Patients Receiving CCRT for Locally Advanced HNSCC
Status:
RECRUITING
Status Verified Date:
2023-04
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
MIT-001
Brief Summary:
The proposed study in patients with previously untreated locally advanced head and neck squamous cell carcinoma HNSCC is designed to evaluate the efficacy and safety of three different doses of MIT-001 compared to the placebo in prevention of oral mucositis OM in patients with HNSCC who are undergoing concurrent chemoradiotherapy CCRT
Detailed Description:
Oral mucositis associated with cancer therapy carries a significant morbidity OM is a common complication in patients receiving CCRT used for treating HNSCC Mucositis lesions can be painful affect nutrition and quality of life QoL and have a significant economic impact However a definitive intervention regime has not been established Therefore it is essential to develop appropriate treatment
MitoImmune Therapeutics Inc hereafter referred to as Sponsor has developed MIT-001 which can scavenge abnormal levels of reactive oxygen species ROS enabling the cells to retain mitochondrial membrane permeability and mitochondrial function This eventually inhibits additional ROS production indicating that MIT-001 can prevent excessive inflammation caused by ROS In addition MIT-001 may possibly 1 block inflammatory cytokine production via inhibiting nuclear factor kappa B NF kB or inflammasome dependent pathways 2 inhibit necrosisnecroptosis via blocking high mobility group box 1 HMGB1 mediated cytokine production and 3 balance regulation between T helper type 117 Th117 and regulatory T cells
Based on the pathophysiological progression of CCRT-associated OM initiated by direct injury to basal epithelial cells which experience deoxyribonucleic acid DNA damage and increased ROS levels Sponsor expects the prevention of OM in patients receiving CCRT of locally advanced HNSCC with MIT 001 by effectively scavenging increased ROS induced by CCRT
MitoImmune Therapeutics Inc hereafter referred to as Sponsor has developed MIT-001 which can scavenge abnormal levels of reactive oxygen species ROS enabling the cells to retain mitochondrial membrane permeability and mitochondrial function This eventually inhibits additional ROS production indicating that MIT-001 can prevent excessive inflammation caused by ROS In addition MIT-001 may possibly 1 block inflammatory cytokine production via inhibiting nuclear factor kappa B NF kB or inflammasome dependent pathways 2 inhibit necrosisnecroptosis via blocking high mobility group box 1 HMGB1 mediated cytokine production and 3 balance regulation between T helper type 117 Th117 and regulatory T cells
Based on the pathophysiological progression of CCRT-associated OM initiated by direct injury to basal epithelial cells which experience deoxyribonucleic acid DNA damage and increased ROS levels Sponsor expects the prevention of OM in patients receiving CCRT of locally advanced HNSCC with MIT 001 by effectively scavenging increased ROS induced by CCRT
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
True
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None