Our drug, TRE-515, has a mechanism of action that impacts a wide range of bad-acting cells, reducing their ability to rapidly reproduce. This has the potential to diminish autoimmune flares and slow, or even stop, cancer growth. Our early-stage development pipeline priorities are data-driven, guided by preclinical and clinical progress as well as FDA insights and NIH funding.
Programs in detail
The lead focus is advanced solid tumors, with two featured combination programs. Autoimmune and neurodegeneration programs advance in parallel on the same mechanism.
Clinical: Phase 1A
Advanced Solid Tumors
The ongoing lead program, a US-based, multi-site, Phase 1a, dose escalation trial, successfully reached the maximum tested dose, evaluating TRE-515 as a monotherapy in patients with advanced solid tumors.
Trial Identifier: NCT05055609
Safety
Well tolerated, with no dose-limiting toxicities in any cohort (40 mg to 1440 mg) during dose escalation.
Dose
Rapid oral absorption, over a > 6 hour plasma half-life supporting a once-daily capsule.
Benefit
Multiple patients showed disease control over 200 days, despite aggressive late-stage cancers.
47%
disease control
* 14/30 evaluable patients; RECIST v1.1
$2.0M
NCI grant funded
>35
patients dosed, dose escalation portion complete
Dose exploration and expansion currently underway
Patient One
Stephanie was the first person ever to receive TRE-515. She joined the Phase 1 trial when there was no patient experience with the drug to go on, and she openly shared her experience after months of treatment.
“There are even days that I forget I have cancer.”
“I am able to live more normally. I’m thankful this is an oral medication instead of an infusion. On a daily basis, I’m not as sick feeling, and there are even days that I forget I have cancer. I’m able to travel and drive. I don’t have to have caregivers waiting on me after chemo. With this drug, I feel good the majority of the time.”
Stephanie, first patient to receive TRE-515
* Individual experiences do not establish safety or efficacy
Preclinical: IND Enabling
FDA Fast Track
Prostate Cancer
TRE-515 + Radiation
7 in 10
men show no response to current radioligand therapy
VISION trial (NCT03511664)
~4 months
added survival when it does work
50%+
of prostate cancer patients receive some form of radiation
Radiation therapies work by damaging the DNA of prostate cancer cells, but those cells can use the Salvage Pathway to repair the damage and keep growing. TRE-515 is designed to block that recovery step, with the goal of making proven radiation treatments work better rather than replacing them.
Approach
Combine TRE-515 with radiation, including radioligand therapies such as Pluvicto, in metastatic castration-resistant prostate cancer.
Mechanism
Radiation damages cancer cell DNA. Blocking dCK makes it harder for those cells to replenish the building blocks they need for repair.
Regulatory
Designated as a Fast Track product: TRE-515 in combination with lutetium Lu 177 vipivotide tetraxetan, for prostate-specific membrane antigen (PSMA)-positive metastatic castration-resistant prostate cancer (mCRPC).
Ken Schultz, Chairman and CEO, on TRE-515 and prostate cancer
“We’re not trying to replace therapies that work. We’re trying to make them better.”
Ken Schultz, Chairman and CEO
Preclinical: Proof of Concept
Multiple Sclerosis, Optic Neuritis, Crohn’s Disease, and ADEM
TRE-515 modulates the immune-cell activation that drives disease, with significant improvement demonstrated in mouse models.
FDA Expanded Access Clinical Trial
ALS
Amyotrophic lateral sclerosis, aka Lou Gehrig’s disease
TRE-515 has been made available to ALS patients through the FDA Expanded Access pathway.
* Individual experiences do not establish safety or efficacy