The unique BIOZEUS business model and structure allows taking on a portfolio of promising early development projects, to confirm early data and generate proof of concept in animals and from there, advance them to the clinical phase. 

As BIOZEUS works with a portfolio of projects, the company can terminate projects fast if the data are not promising enough, without putting the company at risk compared to biotech companies focused on one technology. This strategy allow risk mitigation and a very capital efficient development approach, as the company is not centered on one technology.

BIOZEUS develops a portfolio from different therapeutic areas, selected based on high medical need, scientific and commercial criteria and global intellectual property (IP).



          BIOZEUS has currently 3 compounds in active development, of which one is a                    platform technology, split into three subprojects with different indications. 

         All projects and subprojects address high medical needs with high commercial                  potentials.

Timeline Developing Project

imageBZ068: Rheumatoid arthritis

BZ 068 addresses key medical needs in Rheumatoid Arthritis through its unique and novel disease-modifying mechanism of action. BZ068 acts inhibiting synovial fibroblast migration, invasion, and activation, as well as T-lymphocytes proliferation, without causing immunosuppression. BZ068 has a favorable pharmacokinetic profile allowing oral administration. BZ068 would add an exciting new treatment option for Rheumatoid Arthritis and potential other follow up indications.



BZ371 Platform: Nitric Oxide Synthase (NOS) Enhancers

Biozeus is developing a small peptide drug platform of NOS enhancers. NO is reduced with aging and NO deficiency is the main physiopathological mechanism several diseases.

Biozeus’ proprietary small peptide, topical drug, induces local expression of NOS, resulting in endogenous NO production in the target cells, restoring the physiological level of NO.

Based on that mechanism, a platform was created, with different target tissues: Skin, Lung and eye. Although the platform has the potential to address several diseases, some diseases were selected due to the high unmeet medical need. For Skin, erectile dysfunction and psoriasis. For lung: Pulmonary Arterial Hypertension (PAH), COPD and SARS. For eye: Glaucoma and NAION.



Erectile dysfunction (ED)

NO is a potent endogenous vasodilator and it is well know that erection starts with NO production. Dysfunction of NO production is implicated in the ED disease pathophysiology. 

There is still a significant medical need for the patients not attended by PDE5is – those drugs do not act starting erection but it acts by improving/prolonging the erection effect. Therefore 36% of ED patients do not respond to PDE5i due to low/no NO production (like, aging, diabetes hypertension, prostatectomy and spinal cord injury patients). However, the market offers only unattractive treatment alternatives. 

BZ371A, a topical peptide drug, enhances the effect of NOS (iNOS and nNOS) in the penis, resulting in a physiological and local NO production, causing vasodilatation and penile erection without systemic exposure. The NO production does not depend on the endothelial cells (jeopardized in diabetes and hypertension patients) nor on the CNS stimulus (damaged in prostatectomy and spinal cord injury patients).

The local effect without systemic exposure makes BZ371A a safe approach for those PDE5is drop out. BZ371A MOA also allows it to be used in combination with PDE5is, as BZ371A start the erection and PDE5is potentialize/prolong it. This synergistic effect was already proved in animal trials.

Preclinical efficacy and safety package, FDA pre-IND feedback, formulation development and first human exploratory clinical data have been generated.

BZ371A attends the medical needs of currently badly attended ED subgroups like PDE-5i non-responders, contraindicated or dropouts, PDE5i weak responders (to be combined with PDE5i, in a synergistic way), but also the general ED population.



Preservation of Erectile function following radical prostatectomy

161.000 men per year undergo a radical prostatectomy (RP) in the United States due to prostate cancer. Trauma resulting from surgical manipulation of the neurovascular bundles may result in neuropraxia. The neural injury prevents the normal release of NO from the cavernosal nerve endings, which cause atrophy and degradation of the underlying cavernosal smooth muscle (apoptosis followed by excessive collagen deposit), which can lead to definitive erection dysfunction (ED). Less than 15% of patients submitted to RP respond to the oral Phosphodiesterase 5 inhibitors (PDE5i). PDE5is depend on sufficient NO production to act, as they only prolong the effect of NO.  

BZ371A induces local expression of NOS in the penis, resulting in the physiological NO production causing vasodilatation and penile erection. Therefore BZ371A counteract the proapoptotic and profibrotic cascade induced by RP neural injury. 

This is a totally new, potentially more effective and safer approach (limited systemic exposure) to explore the full therapeutical potential of NO following RP. Considering the synergistic effect with PDE5is (one acts upstream the other downstream in the NO pathway), patients also could benefit from the combination. 



Psoriasis and other skin diseases

NO is a powerful molecule that acts like a vasodilator, immune and inflammatory mediator, with excellent anti-bacterial properties, having a central role in cutaneous biology and in many dermatological diseases. Derangement of NO production is implicated in the etiology of a multitude of dermatologic diseases like Psoriasis, Acne, Molluscum Contagiosum and Atopic Dermatitis. Nevertheless, the challenge to develop a safe and constant topical NO delivery system have hampered NO´s therapeutic use systems for dermatological diseases.

BZ371 platform emerges as a solution to this problem, with a novel mechanism of action that translates into a more constant, safer and prolonged supply of NO. Our peptides are safe for topical application and our rational supports two possible therapeutic routes for their application to treat dermatological diseases: (I) as an anti-proliferative agent, with potential to treat psoriasis; and (II) as an antimicrobial and inflammation modulator agent, with potential to treat atopic dermatitis, molluscum contagiosum and/or acne. Nevertheless, there are multiple potential applications of our platform in dermatology, including cosmetic applications.



Glaucoma patients lose vision due to increased intraocular pressure (IOP) that causes retinal ganglion cells die and/or loss of blood flow to the optic nerve head. Aging reduces NO production and some diseases reduce it as well. Evidence indicates that lack of NO is related to glaucoma. NO has become a validated target for the treatment of glaucoma as it relaxes smooth muscle cells, from vessels and the trabecular meshwork, increasing the aquous humor trabecular out flow and increasing the blood flow around the optical nerve head. This is the NO´s pivotal mechanoregulatory role in IOP reduction and neuroprotection. 

BZ371A, a small synthetic peptide, induces physiologic expression of Nitric Oxide Synthase (NOS) in the eye, starting the local production of NO and compensating lack of NO in the glaucoma eye. BZ371A is found on retinal area after one eye drop, but it cannot be found systemically (no systemic exposure). NOS expression lasts for a long period (almost 24h) after one eye drop. This novel mechanism of action, in combination with eye drop application with long effect and no systemic exposure, translates into a more constant, safer and prolonged option.

Significant reduction in IOP, as well as neuroprotective effects, have been shown in animal trials, after single or 28 days repeated topical applications of BZ371A, with a significant preclinical and exploratory/human safety profile 

Therefore, BZ371A is the only drug able to normalize the optic nerve head perfusion, in combination with reducing IOP, treating glaucoma with neuroprotective effect.



NAION and neuroprotection

BZ371A induces the local NO production in the optic nerve heads by enhancing the activity and expression NOS. 

BZ371A is capable of reach the retina with one eye drop application. Both in prevention as in treatment administration, BZ371A one eye drop per day preserves/reduces the histological damage caused by ischemia, preserving the number of retinal ganglion cells (RGC) and the vision.

Non-arteritic ischemic optic neuropathy (NAION) is a rare disease with no treatment approved (very high unmet medical need), caused by ischemia of anterior segment of the optic nerve, leading to the death of RGC. NO acts in some neurotoxicological pathophysiologies: (i) NO is a vasodilator, increasing locally the blood flow, and therefore acting against ischemia;  (ii) NO can downregulate the NMDA receptor (the glutamate binding receptor), and therefore reduce the excitotoxicity; (iii) NO can act as a scavenger, consuming the free radicals, and therefore reducing the oxidative stress.

On the other hand, both overexpression as well as underexpression of NO could contribute to nerve damage. Therefore a therapeutic approach, capable of restoring the NO physiology in a controlled manner, is very desirable, as BZ371A presents.