NOVATEK PHARMACEUTICALS

What we do

Overview

Novatek Pharmaceutical was created to develop and commercialize an innovative therapeutic approach to treat COVID-19. In other words, our product was driven by wanting to provide effective results to offer great health benefits with quality that lives up to the highest standards. 

Novatek Pharmaceuticals Black seed oil is a natural product with therapeutic potential in management of SARS-CoV-2 due to its anti-viral activity. Derived from Nigella Sativa plant, it has been extensively studied and shown to possess a wide spectrum of activities which include antibacterial, antifungal and antiviral effects among many others. Most of the therapeutic properties are due to thymoquinone, a major bioactive constituent of N. sativa seeds.

Thymoquinone may block the SARS-CoV-2 entry via ACE2 in pneumocytes. N. sativa oil and thymoquinone produce antinociceptive effects through indirect activation of supraspinal μ1- and κ-opioid receptor subtypes. In addition, brain endogenous angiotensin II is involved in central nociceptive mechanisms by its antagonistic interaction with the endogenous opioid system. It has been shown that opioid active peptides such as hemorphins have inhibitory effect on ACE. This line of evidence suggests that opioid receptors and ACE share similar inhibitory molecules; and, as such, it is possible that thymoquinone might also block ACE2.

Near term milestones include completion of a Phase 2 clinical study to support possible FDA Emergency Use Authorization to treat non-hospitalized SARS-CoV-2 positive patients with mild to moderate COVID-19 infection with corresponding symptoms.

Technology Overview

  • Coronaviruses contain specific genes that encode proteins for viral replication, nucleocapsid and spike formation. Glycoprotein spikes on the surface are responsible for attachment and entry to host cells. MERS-coronavirus uses dipeptidyl peptidase 4 (DPP4), while HCoV-NL63 and SARS-coronavirus require angiotensin-converting enzyme 2 (ACE2) as a key receptor. Many host-cell receptors are recognized by the viral spike of SARS-Cov-2.

  • In the host, the virus life cycle consists of 5 steps: attachment, penetration, biosynthesis, maturation and release. Once viruses bind to host receptors, they enter through endocytosis or membrane fusion. Viral contents are released, viral RNA enters the nucleus for replication and new viral particles are released. Coronaviruses consist of 4 structural proteins; Spike (S), membrane (M), envelop (E) and nucleocapsid (N). The spike has two functional subunits; S1 is responsible for binding to the host cell receptor and S2 for fusion of the viral and cellular membranes.

  • Symptoms of patients infected with SARS-CoV-2 range from mild to severe respiratory failure with multiple organ failure. Because ACE2 is highly expressed on the apical side of lung epithelial cells in the alveolar space, this virus can enter and destroy them. This matches with the fact that the early lung injury is often seen in the distal airway. Patients with severe diseases show lymphopenia, particularly reduction in peripheral blood T cells.

  • Thymoquinone may block the SARS-CoV-2 entry via ACE2 in pneumocytes. N. sativa oil and thymoquinone produce antinociceptive effects through indirect activation of supraspinal μ1- and κ-opioid receptor subtypes. In addition, brain endogenous angiotensin II was involved in central nociceptive mechanisms by its antagonistic interaction with the endogenous opioid system. Furthermore, it has been shown that opioid active peptides such as hemorphins have inhibitory effect on ACE. This line of evidence suggests that opioid receptors and ACE share similar inhibitory molecules and as such it is possible that thymoquinone might also block ACE2.
  • Coronaviruses contain specific genes that encode proteins for viral replication, nucleocapsid and spike formation. Glycoprotein spikes on the surface are responsible for attachment and entry to host cells. MERS-coronavirus uses dipeptidyl peptidase 4 (DPP4), while HCoV-NL63 and SARS-coronavirus require angiotensin-converting enzyme 2 (ACE2) as a key receptor. Many host-cell receptors are recognized by the viral spike of SARS-Cov-2.

  • In the host, the virus life cycle consists of 5 steps: attachment, penetration, biosynthesis, maturation and release. Once viruses bind to host receptors, they enter through endocytosis or membrane fusion. Viral contents are released, viral RNA enters the nucleus for replication and new viral particles are released. Coronaviruses consist of 4 structural proteins; Spike (S), membrane (M), envelop (E) and nucleocapsid (N). The spike has two functional subunits; S1 is responsible for binding to the host cell receptor and S2 for fusion of the viral and cellular membranes.

  • Symptoms of patients infected with SARS-CoV-2 range from mild to severe respiratory failure with multiple organ failure. Because ACE2 is highly expressed on the apical side of lung epithelial cells in the alveolar space, this virus can enter and destroy them. This matches with the fact that the early lung injury is often seen in the distal airway. Patients with severe diseases show lymphopenia, particularly reduction in peripheral blood T cells.

  • Thymoquinone may block the SARS-CoV-2 entry via ACE2 in pneumocytes. N. sativa oil and thymoquinone produce antinociceptive effects through indirect activation of supraspinal μ1- and κ-opioid receptor subtypes. In addition, brain endogenous angiotensin II was involved in central nociceptive mechanisms by its antagonistic interaction with the endogenous opioid system. Furthermore, it has been shown that opioid active peptides such as hemorphins have inhibitory effect on ACE. This line of evidence suggests that opioid receptors and ACE share similar inhibitory molecules and as such it is possible that thymoquinone might also block ACE2.

Technology Overview

Technology Overview

  • Coronaviruses contain specific genes that encode proteins for viral replication, nucleocapsid and spike formation. Glycoprotein spikes on the surface are responsible for attachment and entry to host cells. MERS-coronavirus uses dipeptidyl peptidase 4 (DPP4), while HCoV-NL63 and SARS-coronavirus require angiotensin-converting enzyme 2 (ACE2) as a key receptor. Many host-cell receptors are recognized by the viral spike of SARS-Cov-2.

  • In the host, the virus life cycle consists of 5 steps: attachment, penetration, biosynthesis, maturation and release. Once viruses bind to host receptors, they enter through endocytosis or membrane fusion. Viral contents are released, viral RNA enters the nucleus for replication and new viral particles are released. Coronaviruses consist of 4 structural proteins; Spike (S), membrane (M), envelop (E) and nucleocapsid (N). The spike has two functional subunits; S1 is responsible for binding to the host cell receptor and S2 for fusion of the viral and cellular membranes.

  • Symptoms of patients infected with SARS-CoV-2 range from mild to severe respiratory failure with multiple organ failure. Because ACE2 is highly expressed on the apical side of lung epithelial cells in the alveolar space, this virus can enter and destroy them. This matches with the fact that the early lung injury is often seen in the distal airway. Patients with severe diseases show lymphopenia, particularly reduction in peripheral blood T cells.

  • Thymoquinone may block the SARS-CoV-2 entry via ACE2 in pneumocytes. N. sativa oil and thymoquinone produce antinociceptive effects through indirect activation of supraspinal μ1- and κ-opioid receptor subtypes. In addition, brain endogenous angiotensin II was involved in central nociceptive mechanisms by its antagonistic interaction with the endogenous opioid system. Furthermore, it has been shown that opioid active peptides such as hemorphins have inhibitory effect on ACE. This line of evidence suggests that opioid receptors and ACE share similar inhibitory molecules and as such it is possible that thymoquinone might also block ACE2.

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