News & Trends - Pharmaceuticals
MSD and Qbiotics collaborate to advance melanoma therapy

Pharma News: QBiotics, an Australian life sciences company developing novel anticancer and wound healing pharmaceuticals, has entered into an agreement with MSD to evaluate use of its lead molecule tigilanol tiglate, in combination with Keytruda (pembrolizumab) in patients with unresectable melanoma.
Dr Victoria Gordon, Managing Director and CEO of QBiotics, said, “We are delighted to announce this collaboration with MSD. Patients with unresectable melanoma who have received prior checkpoint inhibitors currently have limited effective treatment options. Through this program we hope to see that when combined, tigilanol tiglate and Keytruda may produce additive anti-tumour immune responses, and improve outcomes for patients.”
The Phase I/II open label ‘QBC46-H06’ study is a dose escalation and expansion study with the primary objective of determining the maximum tolerated dose or maximum feasible dose of the combination therapy. Secondary measures include assessing tumour responses in both injected tumours and uninjected tumours, as well as clinical efficacy parameters. Patients with unresectable melanoma and who have had exposure to immune checkpoint inhibitors are eligible for the study.
Dr Gordon continued, “This study follows on from encouraging Phase I data where tigilanol tiglate as a monotherapy showed a 27% treatment response rate, including an 18% complete response with full tumour destruction across a wide variety of solid tumour types. Two patients with melanoma that had complete responses also had an abscopal (anenestic) response. Melanoma is the second human application we are pursuing for tigilanol tiglate following on from our Phase I/II clinical trial in patients with Head and Neck Squamous Cell Carcinoma (HNSCC) which commenced in December 2019”.
Tigilanol tiglate is a small molecule administered by intratumoural injection directly into the solid tumour mass. Once injected, it has a multi-modal action including (i) rapid, but highly localised, inflammatory responses, (ii) increased permeability and destruction of tumour vascular endothelium, and (iii) rapid tumour cell death by oncosis.
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