Avid Bioservices Inc (CDMO)

[biopharm]

That is false, there are big milestone payments and Omeros has Breakthru Designation given already from FDA for PS Targeting and BLA filed : )

Hold those shares of Avid CDMO because new IIS have other information that you may not be privy to

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Sept 10, 2019

Omeros Corporate Presentation

Pg6 (read all ...just highlighting)

"Phosphatidylserine(PS) is a newly discovered GPR174 agonist."

"Represents a new axis in cancer Immunotherapy for all solid tumors"

"Could address non-responders to all current therapies"

READ all 51 pages of Corportate Presentation and PS is STRESSED as high importance and BLA filed / Breakthru Designation already accepted ....says NO MORE patients required / BLA data significant

https://investor.omeros.com/static-files/32f2f111-fc8f-47ec-b3ec-4a8a3ef931ac

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Omeros, FDA Agree On Endpoint For Pivotal Trial Of Small Blood Vessel Damage Treatment

Omeros announced Thursday ahead of the market open that it has reached an agreement with the FDA on the response-based primary endpoint of its pivotal trial to support the biologic license application for narsoplimab.

Narosoplimab, codenamed OMS721, is Omeros' lead human monoclonal antibody candidate for the treatment of hematopoietic stem cell transplant-associated thrombotic microangiopathy, or HSCT-TMA.

HSCT-TMA is a severe complication of HSCT, affecting about 20-30% of recipients. TMA is a condition where small blood vessels are damaged due to an endothelial injury, which in turn affects key organs such as the brain, kidney and heart.

Why It's Important

HSCT-TMA has no approved treatment, and narsoplimab is the only drug in development for the condition. The investigational asset has been granted Breakthrough Therapy Designation.

Omeros expressed confidence that the study will meet the primary endpoint.

What's Next

Omeros said it will now complete the ongoing data collection from medical records of patients already treated with narosplimab either in the clinical trial or under compassionate use for inclusion in the clinical sections of the BLA.

It also plans to meet with the European Medicines Agency's rapporteurs this summer to pave the way for European approval.

The company hopes to complete and submit the BLA, as well as the MAA for European approval.

Omeros has the leeway to make a rolling submission to the FDA, which allows it to submit the completed portions without having to wait for all the sections to be completed.

https://m.benzinga.com/article/14060738

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Narsoplimab (OMS721)
Narsoplimab is a human monoclonal antibody targeting mannan-binding lectin-associated serine protease-2 (MASP-2), the effector enzyme of the lectin pathway of the complement system. The lectin pathway is one of the principal pathways of complement and is activated primarily by tissue damage and microbial infection. Importantly, inhibition of MASP-2 does not appear to interfere with the classical complement pathway, a critical component of the acquired immune response to infection. This novel, proprietary drug is designed to prevent complement-mediated inflammation and endothelial damage while leaving intact the respective functions of the other pathways of innate immunity.
HEMOTOPOIETIC STEM CELL TRANSPLANT-ASSOCIATED THROMBOTIC MICROANGIOPATHY (HSCT-TMA)
Narsoplimab has been granted FDA Breakthrough Therapy designation in patients who have high-risk HSCT-TMA, as well as Orphan Drug designation for the prevention of complement-mediated TMAs and for the treatment of HSCT-TMA. In the European Union, narsoplimab has been designated an Orphan Medicinal Product for treatment in hematopoietic stem cell transplantation.
In a late-stage clinical trial compared to an historical control, narsoplimab improved the estimated median overall survival in high-risk HSCT-TMA patients by an order of magnitude and improved 100-day survival by approximately six-fold.
With the FDA’s only Breakthrough Therapy designation awarded for this disorder, as well as Orphan Drug designations from both the FDA and the European Medicines Agency, we currently are preparing marketing applications for the approval of narsoplimab in both the US and Europe to treat HSCT-TMA.

IgA NEPHROPATHY
Narsoplimab has also received FDA Breakthrough Therapy and Orphan Drug designations for the treatment of IgA nephropathy and Orphan Medicinal Product designation for IgA nephropathy in the European Union.
In a Phase 2 clinical trial, narsoplimab reduced proteinuria in IgA nephropathy patients by 50%-90% and stabilized or increased glomerular filtration rates – effects unmatched by any other drug in development for IgA nepropathy.
With the FDA’s only Breakthrough Therapy designation awarded for this disorder, as well as Orphan Drug designations from both the FDA and the European Medicines Agency, narsoplimab is advancing through a Phase 3 clinical program to treat IgA nephropathy.

ATYPICAL HEMOLYTIC UREMIC SYNDROME (aHUS)
Narsoplimab has received FDA Fast Track designation for the treatment of aHUS. Phase 2 clinical results are positive and a Phase 3 clinical program is underway.

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Now there is ample evidence that flipped PS to increases and exists in IgA nepropathy as Omeros has discovered / along with other oncology indications / with one example seen below detailing other research
......

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Increased phosphatidylserine-exposing microparticles and their originating cells are associated with the coagulation process in patients with IgA nephropathy.

He Z, et al. Nephrol Dial Transplant. 2016.

Authors
He Z1, Zhang Y2, Cao M2, Ma R2, Meng H3, Yao Z2, Zhao L2, Liu Y2, Wu X2, Deng R2, Dong Z4, Bi Y4, Kou J3, Novakovic V5, Shi J2, Hao L1.
Author information
1
Department of Nephropathy and Hemodialysis, First Hospital, Harbin Medical University, Harbin, China.
2
Department of Hematology, First Hospital, Harbin Medical University, Harbin, China.
3
Department of Cardiology, Second Hospital, Harbin Medical University, Harbin, China.
4
Department of Cardiology, First Hospital, Harbin Medical University, Harbin, China.
5
Research Department, VA Boston Healthcare System, Boston, MA, USA.
Citation
Nephrol Dial Transplant. 2016 May;31(5):747-59. doi: 10.1093/ndt/gfv403. Epub 2015 Dec 15.
Abstract
BACKGROUND: Relatively little information is available about phosphatidylserine positive (PS(+)) microparticles (MPs) and their originating cells in IgA nephropathy (IgAN) despite well-established intraglomerular coagulation. Our objectives were to detect PS exposure on MP membranes and MP-origin cells and to evaluate its role in procoagulant activity (PCA) and fibrin formation and their association with pathological lesions in the disease.

METHODS: Patients with IgAN and healthy controls were studied. Lactadherin was used to quantify PS exposure on MPs and MP-origin cells. PCA of MPs and MP-origin cells was evaluated by clotting time and purified coagulation complex assays. Fibrin production was determined by turbidity. PS exposure, fibrin strands and FVa/Xa binding were observed on MPs/cells using confocal microscopy.

RESULTS: Using flow cytometry, we found that IgAN patients had high levels of PS(+) MPs derived from lymphocytes, monocytes, neutrophils, platelets, erythrocytes and endothelial cells (ECs). The PS exposure on MP-origin cells also increased in these patients. MPs and MP-origin cells (leukocytes, platelets and erythrocytes) isolated from IgAN patients and ECs cultured with IgAN serum had a significantly shorter median coagulation time (P < 0.001), higher median intrinsic FXa (P < 0.001) and higher thrombin (P < 0.001) generation than controls. These coagulation functional assays were associated with the glomerular lesions. The lesions were also correlated with glomerular fibrin deposition (all P < 0.05). In the presence of patient MPs or their related cells, fibrin formation peaked faster with a higher maximum turbidity when compared with healthy controls. Blocking PS with lactadherin in the IgAN group prolonged coagulation time to control levels, inhibited the PCA up to 80% and markedly reduced fibrin formation. More importantly, we observed that fibrin strands formed on MPs and ECs in the same regions that bound lactadherin, similar to the FVa/Xa costaining.

CONCLUSIONS: We find that high levels of PS(+) MPs and the MP-origin cells are associated with the coagulation process in IgAN, and this may provide a previously unrecognized contribution to intraglomerular coagulation.

https://www.ncbi.nlm.nih.gov/m/pubmed/26673909/

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