TASK ORDER TITLE: PREVENTING LUNG ADENOCARCINOMA (LUAD) USING TRAIL INDUCING AGENT, ONC201BASE CONTRACT TITLE: PREVENT PRECLINICAL DRUG DEVELOPMENT

NIH RePORTER · NIH · N01 · $982,258 · view on reporter.nih.gov ↗

Abstract

Lung cancer is the leading cause of cancer mortality in the US and worldwide. Of the two main histopathological types of lung cancer, non-small cell lung cancer (NSCLC) - which includes adenocarcinoma (AC) and squamous cell carcinoma (SCC) - comprises approximately 85% of all lung cancer patients while small cell lung cancer (SCLC) makes up the remaining 15%. KRAS mutations are found in ~25% of lung adenocarcinomas (LUADs), EGFR mutations are seen in ~15% of LUADs, and the remaining are small percentages of other mutations. At present, the 5-year survival rate of lung cancer is <20%, thus, underscoring preventive strategies including smoking cessation and secondary preventive approaches for high-risk individuals with atypical lung nodules with hyperplasia and adenomas. ONC201 (TIC10) is a selective antagonist of dopamine receptor D2 that reduces cell proliferation and induces TNF-related apoptosis inducing ligand (TRAIL)-mediated apoptosis via integrated stress response activation and AKT/ERK inactivation. It is highly specific for cancer cells, having no effect on normal cells at concentrations that inhibit cancer cell growth. ONC201 is orally available and has demonstrated a favorable safety profile in rats and dogs, as well as in Phase 1 trials in advanced solid tumors. In the Phase 1 trials, ONC201 was administered at doses up to 625 mg once weekly for 3 weeks. No drug-related toxicities greater than grade 1 were reported, the dose was well tolerated, and displayed favorable pharmacokinetic properties in trial subjects. ONC201 is currently being tested in several Phase 2 trials (e.g., NCT03034200, NCT03295396, NCT03485729, NCT02525692, and NCT04055649). Preliminary studies with ONC201 have shown that ONC201 suppresses the lung tumor growth of A549 xenografts in SCID mice in a dose-dependent manner. Both the tested doses (10 and 50 mg/kg ONC201) did not affect the body weights of treated mice and significantly increased TRAIL and Death Receptor 5 (DR5) protein levels while inactivating Akt- Erk signaling. The purpose of this Task Order is to determine the potential clinical usefulness of ONC201 in preventing high risk LUAD in preclinical models.

Key facts

NIH application ID
10705393
Project number
75N91019D00020-0-759102200003-1
Recipient
UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR
Principal Investigator
CHINTHALAPALLY RAO
Activity code
N01
Funding institute
NIH
Fiscal year
2022
Award amount
$982,258
Award type
Project period
2022-09-08 → 2025-09-07