Novel Monoclonal Antibodies for Immune and Inflammatory Diseases

We are advancing first-in-class therapies, including EB05 (Paridiprubart), that target critical points in inflammatory and innate immune response pathways. Our goal is to transform the lives of patients suffering from acute and chronic diseases.


First in Class mAb

Our most advanced drug candidate is EB05 (Paridiprubart), a monoclonal antibody developed for acute and chronic disease indications that involve dysregulated innate immunity responses.


Well Documented Mechanism of Action

EB05 (Paridiprubart) dampens TLR4 signaling by blocking receptor dimerization and has been shown to be independent of ligand type and concentration.


Fast Tracked by FDA

To receive Fast Track, drug candidates must treat a serious disease and have non-clinical/clinical data that demonstrate the potential to address an unmet medical need.

Without EB05 (Paridiprubart)

With EB05 (Paridiprubart)

Without EB05 (Paridiprubart)

With EB05 (Paridiprubart)

Toll-like receptor 4 (TLR4) – a key component of the innate immune system and an important mediator of inflammation. Since TLR4 detects molecules found in pathogens and also binds to endogenous molecules produced as a result of injury, it is a key receptor on which both infectious and noninfectious stimuli converge to induce a proinflammatory response. Specifically, TLR4 signaling activates leukocytes to secrete proinflammatory cytokines (i.e., CXCL10, IL-6, IFN-b, IL-1b, TNF-α), which under certain circumstances can result in a “cytokine storm” – a severe immune reaction.

Acute Respiratory Distress Syndrome (ARDS)

A Leading Cause of ICU Admissions Globally

Life-threatening form of respiratory failure

  • Exaggerated immune response
  • Inflammation and injury to the lungs
  • Edema that deprives the body of oxygen


  • Infections by virus (i.e. Covid-19, influenza) or bacteria, smoke/chemical inhalation and chest injury

Standard of Care

  • Few meaningful treatments, other than supplemental oxygen and mechanical ventilation
  • Substantial evidence that multiple causes of ARDS are mediated by the TLR4 pathway

ARDS – A Significant Disease Burden

Annual Cases Globally


ICU Mortality Rate

$ Cost Per Patient (Average U.S.)

Sars-CoV2 and Other Pathogens

Experts believe that the Sar-CoV2 virus, combined with influenza and other pathogens, will continue to drive ARDS case counts higher.

Ageing Population

Changing demographics increase the risk of developing ARDS. There’s an increasing long-term need for effective ARDS therapeutics.

Co-morbidities and Risk Factors

Increasing incidence of comorbidities and risk factors, including hypertension, diabetes & obesity, can further drive incidence of ARDS

EB05 (Paridiprubart) Decreases Mortality by 84% in Critically Severe Patients

Phase 2 Results

Statistically Significant Mortality Trend in Critical Patients

28-Day Mortality Rate by Treatment Group*

n=33; p=0.04

“Achieving statistical significance in the most difficult-to-treat patients has increased our excitement and belief that Paridiprubart could become a standard-of-care treatment option.”

Par Nijhawan, MD

CEO, Edesa Biotech

Critically ill patient population*

  • 28-day death rate of 7.7% (1/13) in the EB05 (Paridiprubart) arm vs. 40.0% (8/20) in the placebo arm
  • 84% reduction in the risk of dying (HR: 6.12 placebo vs. EB05 (Paridiprubart); 95% CI: 0.77-49.06; p=0.088).
  • All patients received Standard of Care (SOC): ~85% received dexamethasone (or other steroids); >40% received both tocilizumab and a steroid; well balanced

Favorable Safety Profile

  • Paridiprubart, an anti-TLR4 antibody candidate, has been evaluated in multiple clinical studies (with 600+ subjects in total)

*World Health Organization’s Covid-19 Severity Scale Level 7 critically severe patients, receiving extracorporeal membrane oxygenation (ECMO), invasive mechanical ventilation plus organ support, or both. ITT= Intend to Treat (i.e., no randomized subjects were excluded).

EB01- A Topical Daniluromer Formulation for Allergic Contact Dermatitis

Image of Topical Cream Being Applied to Rash on Hand

First-in-Class Anti-Inflammatory

EB01 (daniluromer) is designed to inhibit the inflammatory process at its inception rather than after inflammation has occurred.


Alternative to Steroids

Due to its non-steroidal mechanism of action, Edesa is evaluating EB01 as a treatment for patients with chronic moderate-to-severe Allergic Contact Dermatitis.

Broad Potential Opportunities

Potential for treating treating diverse range of  inflammatory/allergic conditions.


Daniluromer’s Novel Mechanism of Action

sPLA2 inhibitors represent a novel approach treating inflammation without the safety concerns of current therapies

Upstream Modulation

Daniluromer is a new chemical entity that exerts its anti-inflammatory activity through the inhibition of certain pro-inflammatory enzymes known as secretory phospholipase 2, or sPLA2.

Efficacy and Durability

EB01 (daniluromer) has demonstrated efficacy for the treatment of ACD in multiple clinical trials.

Well Tolerated

Daniluromer preserves cell membrane integrity leading to a better safety profile.

Daniluromer inhibits sPLA2 from degrading phospholipids to produce arachidonic acid. Arachidonic acid is processed via the LOX-COX pathway to produce several pro-inflammatory signaling molecules.  Daniluromer exerts its anti-inflammatory activity upstream of currently approved NSAIDs, which target the LOX-COX pathway.

Allergic Contact Dermatits (ACD)

The Leading Occupational Health Issue Related to Dermatology

Type IV, or Delayed-Type, Hypersensitivity Reaction

  • Immune system sensitized following initial contact with allergen
  • Subsequent contact results in cell-mediated allergic response at the point of contact
  • Often highly visible on face and hands

Standard of Care

  • No labelled products available
  • Corticosteroids cannot be used for prolonged periods due to safety concerns

Few Treatment Options for Chronic ACD Patients

Known Contact Allergens


Unable to Identify Causal Allergen

No Known Labelled Drugs

ACD Adversely Impacts the Workplace

  • Loss of Productivity
  • Complexitiy of Mitigation
  • Lost Income and Disability Claims

Corticosteroids and Immunomodulators

  • Safety Concerns
  • Side Effects

Physicians strongly desire additional treatment options**

ACD…can make you quit your job.”

“Maybe topical steroids help a little but I almost never use them”

“Topicals are easier to use and they are a safer option than oral medications.”

1.0% EB01 Met Primary and Secondary Endpoints with Statistical Significance

Phase 2B – Preliminary Topline Results of EB01

For the treatment of chronic moderate-to-severe allergic contact dermatitis

Total CDSI Score*

Mean Percent Improvement from Baseline

Total ISGA Score*

% Patients with a ≥2 Point Improvement from Baseline

“We are pleased that the study findings demonstrated that the 1.0% EB01 cream helped patients with moderate-to-severe disease significantly reduce their symptoms and achieve clear or almost clear skin in more than half the cases. A significant improvement was evident as early as two weeks from initiation of treatment.”

Par Nijhawan, MD

CEO, Edesa Biotech


  • 1.0% EB01-treated patients demonstrated a relative improvement of >50% (CDSI) and >80% (ISGA) over placebo/vehicle

Response at 15 Days (CDSI)

  • 44% for 1.0% EB01 vs. 29% for placebo; p=0.05

Response at Follow Up (CDSI)

  • 64% for 1.0% EB01 vs. 44% for placebo; p=0.04

Lowest Efficacious Dose

  • 1.0% EB01 was identified as the lowest efficacious dose over 2.0% and 0.2%


  • No serious treatment-related adverse events were reported across all doses

*Intention to Treat (ITT) population; statistical analysis based on last observation carried forward (LOCF). Placebo (n=84); 1.0% EB01 Cream (n=19). Contact Dermatitis Severity Index (CDSI) at Day 29. Success on the Investigator’s Static Global Assessment (ISGA) is defined as a 2-point reduction and score indicating clear/almost-clear skin. Topline study data are preliminary and subject to change.

** Company sponsored research, including interviews of Key Opinion Leaders

Further Reading

Jiang et al., 2005: TLRs are known to be involved in exaggerated immune responses, with TLR4 shown to induce inflammatory responses that can lead to acute lung injury (ALI) and ARDS

Imai et al., 2008: This study looked at the role of TLR4 in ALI. Mice deficient in TLR4 were resistant to acid-induced ALI and while H5N1 influenza rapidly induced ALI in wild-type mice, TLR4 deficient mice were resistant to H5N1-induced ALI, suggesting a causative role for TLR4 in

Shirey et al., 2016: In this study, an anti-TLR4 antibody protected mice from lethal influenza

Perrin-Cocon et al., 2017: A novel small molecule TLR4 antagonist (FP7) was tested in an in vivo mouse model of influenza. FP7 blocked TLR4 stimulation and protected mice from influenza-induced lethality and reduced inflammatory cytokine expression and

Zhou et al., 2018: An anti-TLR4 monoclonal antibody was studied in a rat model of ARDS. The rats treated with the anti-TLR4 antibody showed lower respiratory frequency, lung permeability, lung edema, inflammatory infiltration, and tumor necrosis factor and interleukin expression levels in lungs along with lower TLR4, TLR9, MyD88, and nuclear factor expression in macrophages.

Domitrovic 2018: TLR4 monoclonal antibodies were evaluated both in vitro and in a rat model of ARDS. Stimulating macrophages with TNF-alpha along with anti-TLR4 antibody eliminated the upregulation and secretion of cytokines. Pre-treating rats with anti-TLR4 antibody prior to ventilation.

Lee et al., 2009: CXCL10 plays a significant role in leukocyte recruitment to inflamed tissues, and because of this it can lead to excessive inflammation and tissue damage. Patients who suffer from ARDS are known to exhibit unusually high levels of CXCL10.

Wang et al., 2013: This study showed that patients suffering from ARDS caused by H1N1 infection had significantly elevated levels of CXCL10 in their serum compared to a control group. An anti-CXCL10 monoclonal antibody increased survival time, reduced lung edema, and significantly decreased ALI in a mouse model of H1N1 infection.

Ichikawa et al., 2013: In this study, ARDS was induced in mice by both non-viral and viral means. Mice deficient in CXCL10 or CXCR3 had improved severity and survival of both viral and non-viral ARDS.

Lang et al., 2017: This study explored the role of CXCL10 in a rat model of LPS-induced ARDS. Expression of CXCL10 and CXCR3 increased after LPS-induction. An anti-CXCL10 antibody decreased the severity of ARDS.

Global Agreement

Edesa has established a strategic global agreement with Light Chain Bioscience, a leading Swiss pharmaceutical development company. Light Chain has been at the forefront of antibody development technology for the last two decades and is a world leader in antibody engineering,

Yissum Collaboration

Edesa collaborates with researchers at Hebrew University of Jerusalem and has a license agreement with the university’s tech transfer agent Yissum Research Development Company for our investigational medicines EB01 and EB02.