Our products

The Company has created and continues to develop a rich pipeline of proprietary, flexible, tumour-targeting drug delivery systems with the potential to deliver new or existing and highly potent drugs within a pro-drug vehicle.

This pipeline of new drug candidates utilises unique mechanisms of action. The tumour is specifically targeted, identified and located. Once achieved the novel mechanism releases the active ‘warhead’, thus reducing side effects due to systemic contamination.

It is also believed that Incanthera drugs could be used as a first wave therapy to initiate tumour cell kill once a solid tumour cancer has been diagnosed. The Incanthera programs have the potential to increase the therapeutic window where such oncology treatments can be utilised.

Scheduled for clinical trials

The Company’s current lead product and focus is Sol, which the Company acquired in September 2018. Sol is a potentially innovative topical product for the treatment of solar keratosis and the prevention of skin cancers. This has achieved proof of concept and is currently being prepared for licensing to a commercial partner within 12-18 months.

The Company commissioned an independent proof of principle study conducted at the University College London School of Pharmacy in Summer 2019.The study, using human skin penetration models, demonstrated that the Company’s advanced formulation technology exceeds the bioequivalence test, which confirms that the Company is able to deliver a topical product for the prevention of actinic keratosis and skin cancer.

The Company’s current lead product and focus is Sol, which the Company acquired in September 2018. Sol is a potentially innovative topical product for the treatment of solar keratosis and the prevention of skin cancers. This has achieved proof of concept and is currently being prepared for licensing to a commercial partner within 12-18 months.

The Company commissioned an independent proof of principle study conducted at the University College London School of Pharmacy in Summer 2019.The study, using human skin penetration models, demonstrated that the Company’s advanced formulation technology exceeds the bioequivalence test, which confirms that the Company is able to deliver a topical product for the prevention of actinic keratosis and skin cancer.

Despite advances in targeted therapy over recent years, the treatment of most adult solid cancers remains palliative rather than curative and represents a major unmet need. Solid cancers, particularly aggressively growing ones, are supported by a network of blood vessels. Vascular Disrupting Agents (“VDAs”) were specifically designed to destroy the vascular network, depriving the growing tumour of essential nutrients and thereby killing it. However, their inherent cardiac toxicity is an obstacle to their effective use in the clinic. EP0015 seeks to address this by releasing the VDA only at the tumour site.

Competitive advantage

The ability of EP0015 to target solid tumours has many possible benefits which will be assessed as part of clinical trials, including:

i. Greater efficacy – improved therapeutic index due to targeting and reduced toxicity;

ii. Side-effects – enhanced patient comfort;

iii. Reduced frequency of treatment – potential cost savings; and

iv. Improved life expectancy – desired outcome.

EP0015 has a significant competitive advantage over many current therapeutic approaches, including other anti-vascular agents because of the ability to achieve high tumour drug concentrations without the corresponding systemic and normal tissue toxicities.

EP0015 has been shown to be effective against a wide range of cancer cells, including the major solid tumours, both in vivo and in vitro. Importantly, EP0015 also demonstrates an absence of the toxicity associated with previous vascular targeting agents.

EP0015 is close to the First Time in Man (FTIM – a clinical phase 1 design in patients) stage and is the subject of commercial agreements with Ellipses Pharma.

Despite advances in targeted therapy over recent years, the treatment of most adult solid cancers remains palliative rather than curative and represents a major unmet need. Solid cancers, particularly aggressively growing ones, are supported by a network of blood vessels. Vascular Disrupting Agents (“VDAs”) were specifically designed to destroy the vascular network, depriving the growing tumour of essential nutrients and thereby killing it. However, their inherent cardiac toxicity is an obstacle to their effective use in the clinic. EP0015 seeks to address this by releasing the VDA only at the tumour site.

Competitive advantage

The ability of EP0015 to target solid tumours has many possible benefits which will be assessed as part of clinical trials, including:

i. Greater efficacy – improved therapeutic index due to targeting and reduced toxicity;

ii. Side-effects – enhanced patient comfort;

iii. Reduced frequency of treatment – potential cost savings; and

iv. Improved life expectancy – desired outcome.

EP0015 has a significant competitive advantage over many current therapeutic approaches, including other anti-vascular agents because of the ability to achieve high tumour drug concentrations without the corresponding systemic and normal tissue toxicities.

EP0015 has been shown to be effective against a wide range of cancer cells, including the major solid tumours, both in vivo and in vitro. Importantly, EP0015 also demonstrates an absence of the toxicity associated with previous vascular targeting agents.

EP0015 is close to the First Time in Man (FTIM – a clinical phase 1 design in patients) stage and is the subject of commercial agreements with Ellipses Pharma.

Equin is a quinone-based prodrug activated by the enzyme DT-diaphorase (DTD) which itself is over-expressed in many solid tumours including breast, colon, liver, bladder, stomach, the central nervous system (CNS), lung tumours and in melanomas. The expression of DTD is increased up to 80-fold in primary non-small cell lung cancer (NSCLC) relative to normal lung cells and up to 35-fold in NSCLC relative to small cell lung cancer (SCLC) cell lines.

Equin has been designed to overcome limitations associated with previously proposed bio-reductive agents including, stability, solubility, poor efficacy and unsuitable clinical regimes. In preclinical development Equin has showed promising efficacy and an improved pharmacokinetic profile.

Equin is currently undergoing preclinical development and has shown promising efficacy and an improved pharmacokinetic profile.

Equin is a quinone-based prodrug activated by the enzyme DT-diaphorase (DTD) which itself is over-expressed in many solid tumours including breast, colon, liver, bladder, stomach, the central nervous system (CNS), lung tumours and in melanomas. The expression of DTD is increased up to 80-fold in primary non-small cell lung cancer (NSCLC) relative to normal lung cells and up to 35-fold in NSCLC relative to small cell lung cancer (SCLC) cell lines.

Equin has been designed to overcome limitations associated with previously proposed bio-reductive agents including, stability, solubility, poor efficacy and unsuitable clinical regimes. In preclinical development Equin has showed promising efficacy and an improved pharmacokinetic profile.

Equin is currently undergoing preclinical development and has shown promising efficacy and an improved pharmacokinetic profile.

Duo-C focuses upon targeting colorectal cancer using duocarmycins, which are recognised for their extreme cytotoxicity, converted to a prodrug and designed to overcome their intrinsic toxicity and make them manageable and potentially useful in the clinical set up. The prodrug is activated by CYP2W1, a catabolic enzyme over-expressed in colorectal cancer. Results to date show promising prospects for this new class of drug, demonstrating successful delivery of ultra-potent agents with acceptable toxicity profiles.

Duo-C is in the late discovery (lead) phase.

Duo-C focuses upon targeting colorectal cancer using duocarmycins, which are recognised for their extreme cytotoxicity, converted to a prodrug and designed to overcome their intrinsic toxicity and make them manageable and potentially useful in the clinical set up. The prodrug is activated by CYP2W1, a catabolic enzyme over-expressed in colorectal cancer. Results to date show promising prospects for this new class of drug, demonstrating successful delivery of ultra-potent agents with acceptable toxicity profiles.

Duo-C is in the late discovery (lead) phase.