Our Pipeline

Drug Indication Pre-clinical Phase 1 Phase 2
KS-c2 cancer
KS-c2 dementia
LK-BT2 wet AMD

Drug candidate KS-c2

An oral inhibitor of the specific types of inflammation  responsible for driving aggressive cancer growth and neurodegenerative brain conditions including dementia associated with Alzheimer’s and Parkinson’s diseases.

KS-c2 is the only known inhibitor of the sPLA2-hGIIA, vimentin and EGFR axis, three proteins that closely cooperate in regulating a wide range of vital cell functions via gene transcription and which now together have emerged as key players in a wide range of degenerative diseases.
KS-c2 is a uniquely anti-degenerative diseases drug with potential broad reach across multiple diseases of ageing.

KS-c2 & dementia

Dementia is already the leading cause of death in women in developed countries and is poised to become the leading cause of death regardless of gender. Despite this seismic shift in disease management, treatment options for dementia, as with many neuroinflammatory conditions, remain very limited.

  • A neurodegenerative condition robbing people of their independence.
  • Depriving patients of their memory, thinking abilities and normal social behaviors
  • The third largest cause of death in the elderly
  • Associated with variety of diseases including Alzheimer's, Parkinson's and Huntington's Diseases, vascular dementia, Lewy body dementia, frontotemporal dementia and sports-related traumatic brain injury.

Principally the result of misfolded proteins:

  • Proteins are long, string-like strands that need to be folded into a precise shape to work
  • In dementia, certain structural protein critical to brain cell function are first folded correctly, but then unfolded and re-folded incorrectly

Is associated with misfolding of two main types of protein

  • Tau, which accumulates inside the neuron as tau tangles
  • Amyloid, which accumulates outside of the neuron as clumps known as amyloid plaque

Treatments aimed at inhibiting or breaking up amyloid plaque alone have had only limited success. Research attention has now switched to discovering drugs that prevent or break down both amyloid plaques and tau tangles.

Dementia treatment is controversial with opinion divided on which pathological feature is the more significant and more worthy of treatment - amyloid plaques or tau tangles.

Amyloid plaques have dominated thinking to date, but drugs that inhibit amyloid plaques have proven to offer only modest (30%) benefit, slowing down the disease process only when given early in the disease. Treatment also requires ongoing 2-weekly intravenous injections, is associated with unwanted side-effects and the long-term benefit yet to be revealed.

Attention has shifted to drugs that inhibit tau tangles and several are undergoing clinical evaluation but, unlike amyloid which occurs on the outside of the brain cells, anti-tau drugs face the challenge of needing to gain access to brain cells to target the tau tangles. The outcomes of those trials remain unknown.

Filamon regards the amyloid vs tau controversy as symptomatic of the trend to precision medicine and that a more multi-targeted approach would be more rational.

Amyloid, tau and vimentin are all closely related proteins known as microfilaments. All three occur at high levels in the brain where they play diverse roles, but particularly a key role in the structure and function of nerve fibres and the transmission of impulses along those fibres. As a result, all three proteins appear inextricably involved in dementia requiring a multi-targeted approach to treatment.

KS-c2 offers the first-in-class prospect of successfully addressing the formation of both amyloid plaques and tau tangles as well as offering activity against a range of neuro-inflammatory changes more broadly.

Filamon regards its KS-c2/dementia program as an exciting world-first opportunity to test an oral drug that crosses the blood-brain barrier and acts on proteins incriminated in the formation of both amyloid plaques and tau tangles which together serve to block nerve impulses and eventually kill brain cells.

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.


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.