Filamon currently has 3 platform technologies, all linked by the ability to correct malfunctioning major genes involved in chronic inflammatory diseases embracing cancer, autoimmune diseases and neurodegenerative diseases. In particular, doing so in a well-tolerated way that previously had been considered in medical research to be unachievable.
KS-c2 is an oral, cyclic peptide, first-in-class inhibitor of hGIIA-vimentin driven inflammation.
KS-c2 has been designed to block the role of inflammation in driving the growth and spread of cancer through the key role of hGIIA-vimentin in establishing the so-called tumour micro-environment. KS-c2 has the potential to become the first universally used anti-inflammatory in cancer treatment.
KS-c2 is being aimed in particular at early-stage cancer where a strong anti-inflammatory effect, depriving the cancer of its inflammatory pro-growth support structure, is expected to serve to increase the effectiveness of standard chemotherapy and/or radiotherapy and deliver better survival outcomes.
Anti-inflammatory treatment already is a standard part of cancer treatment, with steroids such as prednisolone and dexamethasone helping to reduce swelling and pain caused by inflamed tumours.
However, steroids have two key limitations: (i) while good at relieving swelling and pain, they have little effect on the underlying inflammatory actions driving cancer growth, and (ii) they generally are limited to short-term use because of side-effects including osteoporosis, body edema and immune suppression (an effect particularly contra-indicated in cancer).
Filamon sees KS-c2 as the emerging standard cancer anti-inflammatory drug because of its
(i) effectiveness against the tumour micro-environment, and
(ii) because it lacks steroid side-effects associated, in particular having no known inhibitory effect on the immune system.
KS-c2 is intended for long-term use.
KS-c2 is being tested in cancer patients displaying high blood levels of known biomarkers of inflammation and, while inflammation is a driving force in all forms of cancer, Filamon is targeting cancers of the prostate, lung and large bowel where inflammation is an acknowledged major driver of cancer growth and spread in most patients.
JG-1 is an oral, small molecule, first-in-class inhibitor of Tribbles 2, a major driver of cancer aggression and chemo-resistance in most forms of cancer but particularly prostate, lung, breast and pancreatic cancers, neuroendocrine tumours (NETS) and acute myeloid leukaemia.
JG-1 is being developed in the first instance as a means of reversing resistance in prostate cancer cells to a class of drugs known as androgen receptor signaling inhibitors (ARSIs) that represent the current major form of treatment for aggressive forms of prostate cancer.
One of the key fault lines driving this resistance is excessive activity in cancer cells of the signaling protein, Tribbles 2. Tribbles 2 has proven to be more of a technical challenge to inhibit rather than being undruggable and therefore remains to be tested as a means of re-sensitising cancer cells to chemotherapy.
In prostate cancer, ARSIs are enzalutamide (Xtandi), abiraterone (Zytiga), apalutamide (Erleada) and darolutamide (Nubeqa). Between 15-20% of prostate cancers fail to respond to these drugs from the start, with the remainder (responding cancers) eventually failing to respond generally after 12 months.
With ARSIs currently representing the only treatment providing meaningful survival benefits in aggressive prostate cancer, finding a way of overcoming both inherent (from the start) and acquired (later) resistance to ARSIs has become a major imperative.
JG-1 is the first and only known inhibitor of Tribbles 2 function and this action in animal models has proved effective in overcoming chemo-resistance and restoring the ability of enzalutamide to block the growth of prostate cancer cells.
JG-1 is a repurposed, clinic-ready drug that currently is undergoing a pilot proof-of-concept study in men with prostate cancer that is progressing on treatment with enzalutamide or abiraterone.
KL-BT2-topical is a potential revolutionary treatment of wet age-related macular degeneration (wet AMD), the major cause of vision loss in the elderly, with 1 in 7 people >50 years of age affected. We are confident that KL-BT2-topical has the ability to become treatment of choice of patients and ophthalmologists.
Wet AMD along with diabetic macular edema (DME) is a chronic inflammatory disease caused by growth in the retina at the back of the eye of abnormal blood vessels that leak, causing swelling and resulting vision loss.
Current treatment involves monthly injections directly into the eyeball of drugs that seek to block the development of the leaky blood vessels. While an effective treatment for some, current treatments fail to work in 1 in 3 patients and are non-curative in all others, slowing rather than stopping disease progression. The injections also are associated with side-effects, pain and discomfort which together with the inconvenience of monthly rest-of-life clinic visits lead to about 40% of patients withdrawing from treatment after the first year.
Wet AMD and DME are not simple single-fault diseases - they are complex diseases involving faults in a considerable number of signaling proteins. The limited effectiveness of current drugs relates to their limited action against single faults, leaving the majority of faults untreated.
LK-BT2 is the first known drug that targets 10 different faulty signaling proteins, representing all of the known faults behind this disease.
LK-BT2 also is a small molecule, allowing it to be formulated as an eyedropper dosage form (LK-BT2-topical).
Current method of treatment of wet AMD
LK-BT2-topical proposed method of treatment
ADDICTIVE BRAIN BEHAVIOUR
KL-BT2-oral is a small molecule intended for the treatment of brain addictive behaviour associated with excessive levels of ΔFosB. We believe KL-BT2-oral to be the first drug able to modulate ΔFosB activity in a way that does not jeopardise the essential role of ΔFosB in brain function generally.
The brain's reward system is meant to reinforce survival acts which it does by producing the chemical, dopamine, which then produces a 'satisfaction' response. Addiction results from non-essential acts that result in the dopamine response having a magnitude up to 10x normal levels.
ΔFosB plays a key role in this reward system by activating a large number of genes in brain cells producing 'reward chemicals' such as dopamine. ΔFosB levels rise in response to addictive behaviour involving drugs (opioids, nicotine etc) and anti-social behaviour (gambling etc). More significantly, those levels go on accumulating with repeated stimulation, in turn creating high levels of 'reward chemicals.'
ΔFosB has been regarded as an undruggable target given its critical role in brain function generally
LK-BT2 modulates ΔFosB function indirectly by gene transcription, finally making ΔFosB a druggable target.
Having access to a drug that modulates ΔFosB function puts Filamon in the unique position of being able for the first time to validate ΔFosB as a drug target for the treatment of drug addiction and obsessive-compulsive disorder.