KS-c2 & Cancer
KS-c2 was developed initially as a first-in-class, anti-inflammatory drug for use in oncology, in particular to block the role of the sPLA2-hGIIA, vimentin, EGFR axis in driving the establishment of the tumour micro-environment and its crucial role in sustaining cancer aggression.
Cancer inflammation is a special form of inflammation responsible for driving cancer growth, invasiveness and aggression. It does this through the establishment of the tumour micro-environment, a support structure of blood vessels, fibroblasts, nerve cells and immune cells all dedicated to driving cancer growth
Cancer inflammation responds poorly to current anti-inflammatory drugs and this means that a critically important part of the cancer process remains essentially untreated in most cancer patients. Cancer inflammation is a key missing piece of the cancer treatment process.
There is no pan anti-inflammatory treatment used in oncology because no drug has proved to be both universally effective and safe for long-term use. Filamon believes it has a drug that finally provides an effective and safe way to block inflammation. This is an open market that Filamon estimates to be worth > US$30 Billion p.a.
In that role, KS-c2 has undergone a first-in-human study in men with hormone-sensitive prostate cancer, successfully confirming safety/tolerability and bio-availability of the oral dosage form.
KS-c2 will continue to be developed as an anti-inflammatory treatment in cancer patients in parallel with its development as a treatment for dementia.
KS-c2 next enters a Phase Ib/IIa trial dose-finding safety and preliminary efficacy study in patients with advanced solid cancers who are displaying inflammatory biomarkers.
Drug candidate LK-BT2
An oral, small molecule inhibitor of the specific type of inflammation responsible for diseases affecting the retina and resulting in loss of vision.
Target diseases
Wet Age-Related Macular Degeneration (wet AMD) and Diabetic Macular Oedema (DMO) are the two major causes of blindness in the elderly. Both diseases share the same underlying pathology of the abnormal growth of leaky blood vessels in the macular region of the retina, a region of the eye responsible for sharp, central vision.
Retina
Central vision
Patients with wet AMD and DMO undergo progressively blurred vision due to the physical build-up of blood vessels and the swelling coming from leakage of plasma into the macular. Ultimately it leads to total blindness.
Current treatment
Current treatment involves monthly injections directly into the eyeball of drugs that target the VEGF gene components of the disease process. While VEGF genes are an important contributor to the disease process, they are far from being the only ones and the limited scope of current treatment for such a complex disease means that they fail to work in about 30% of cases, with 'working' meaning slowing down disease progression, not stopping it.
The need for monthly, rest-of-life intra-ocular injections with associated pain and discomfort and side-effects also leads to a high (~40%) patient drop-out rate.
Our Approach
LK-BT2 offers a multi-gene approach intended to broaden the treatment's effect across all parts of the disease process, not just the current focus on the VEGF genes.
LK-BT2 has already in an animal model of wet AMD outperformed the current market leader by a considerable degree, leading us to believe that LK-BT2 has the potential to deliver both higher response rates and more effective treatment in patients.
On top of which, as a small molecule, LK-BT2 offers the prospect of a treatment that avoids the challenge of monthly eyeball injections. Our aim is a more patient-friendly, self-administration either as topically (eye dropper formulation) or orally. Both dosage forms currently are under consideration ahead of a planned first-in-human study in 2025.
