Delving into the Latest Updates on TR-987 with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Glucoprime

+ [3]

Target

TLR2

Action

modulators, stimulants

Mechanism

TLR2 modulators(Toll like receptor 2 modulators), Macrophages stimulants

Therapeutic Areas

Cardiovascular DiseasesSkin and Musculoskeletal DiseasesOther Diseases

Active Indication

Chronic venous insufficiencyVaricose UlcerWounds and Injuries

Inactive Indication-

Originator Organization

Kazia Therapeutics Ltd.

Active Organization

TR Therapeutics, Inc.

Kazia Therapeutics Ltd.

Inactive Organization

Glycotex, Inc.

Drug Highest PhasePhase 3

First Approval Date-

Regulation-

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ABSTRACTGlucans are known to promote wound repair. Noncellulosic β‐glucans are recognized as potent immunological activators. β‐Glucans are generally safe and are known to attenuate the rate of postoperative infection. Glyc101 is a particulate β‐glucan isolated from Saccharomyces cerevisiae. In this study, the hypothesis that Glyc101 regulates wound macrophage function was tested. Glyc101 induced tumor necrosis factor (TNF) α transcription in macrophages isolated from murine wound site. Multiplex assay identified interleukin (IL)‐10 and TNFα as two cytokines that are induced by Glyc101 in human blood monocyte‐derived macrophages. Glyc101‐induced TNFα production was observed to be mediated via the TLR‐2 and dectin‐1 receptors, receptor tyrosine kinases and NFκB activation. In murine wound macrophages, Glyc101 potentiated phorbol 12‐myristate 13‐acetate‐induced respiratory burst. In vivo, implantation of Glyc101‐enriched polyvinyl alcohol‐sponges at the wound‐site induced TNFα expression in macrophages. Consistently, Glyc101 induced TNFα expression in wound‐site macrophages isolated from two patients with chronic wounds. These observations establish the translational significance of the net findings of this study. Activation of wound macrophages by Glyc101 represents one of the potential mechanisms by which this β‐glucan may benefit chronic wounds where inefficient inflammatory response is one of the underlying causes of impaired healing.

100 Deals associated with TR-987

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R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Chronic venous insufficiency	Phase 3	United States	TR Therapeutics, Inc.	01 Nov 2024
Chronic venous insufficiency	Phase 3	Australia	TR Therapeutics, Inc.	01 Nov 2024
Varicose Ulcer	Phase 3	United States	TR Therapeutics, Inc.	01 Nov 2024
Varicose Ulcer	Phase 3	Australia	TR Therapeutics, Inc.	01 Nov 2024
Wounds and Injuries	Phase 3	United States	TR Therapeutics, Inc.	01 Nov 2024
Wounds and Injuries	Phase 3	Australia	TR Therapeutics, Inc.	01 Nov 2024

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


WCD2023	Phase 2	Chronic venous insufficiency	82	TR987® 0.1% gel	ixflrgdovq(bhehgecyqd) = nugidetebe rcjjhhvgsw (unbhxqovye ) View more	Positive	03 Jul 2023
				Placebo gel	ixflrgdovq(bhehgecyqd) = pmuzgmudze rcjjhhvgsw (unbhxqovye ) View more
NCT00656474 (CTgov)	Phase 1/2	Wounds and Injuries	12	GLYC-101 (GLYC-101 Active Retro-auricular Site (1 Per Participant))	xgfosqkqgo(rcvtfyvhid) = pemtoyqvol yugvpkseav (orawsffsqx, adgggkeuug - dgnhmnszcw) View more	-	25 Jul 2011
				Placebo (Placebo Retro-auricular Site (1 Per Participant))	xgfosqkqgo(rcvtfyvhid) = kphrbsoeok yugvpkseav (orawsffsqx, hlgqkfsbye - yqoobbpalf) View more