A Disturbance in the Force
Some info from LinkedIn and a patent that they have shared. It seems the lead compound (EF-022) is a lectin-receptor activator that modulates suppressor macrophages and tolerogenic dendritic cells.dumbcritic said:Dr. Nobuto Yamamoto discovered and characterised this starting in the 90s. He is still alive and in his late 80s or early 90s now.
He sold all his patents to an Israeli company (Efranat) who are conducting a Phase I trial https://clinicaltrials.gov/ct2/show/NCT02052492 They have published some early data from it http://mct.aacrjournals.org/content/14/12_Supplement_2/B30 One of the main reasons they got enough investment was due to the results in dogs they treated who all had spontaneous tumours http://efranat.com/Research-Development1/Canines-Treatment-Results.aspx
First Immune/Immuno Biotech which are based in Guernsey were founded by Dr. Marco Ruggiero and David Noakes. When Efranat brought a vial that allegedly contained the molecule they couldn't find any when it was tested by them http://www.globes.co.il/en/article-cancer-treatment-developer-efranat-raises-45-million-1000987334 Far more worrying is the fact that when the MHRA raided another of First Immune's facilities they found it wasn't up to GMP standards and was unlicensed too. The blood plasma starting material being used to make this stated: ''Not to be administered to humans or used in any drug products.'' https://www.gov.uk/government/news/regulator-warns-against-gcmaf-made-in-unlicensed-facility-in-cambridgeshire
In 25% of patients (n=24) with refractory tumours then it lead to stabilized disease. This was the fourth line of treatment for over a third of them. To be eligible they had to have failed standard of care (chemo, PD-1 inhibitor and/or a EGFR inhibitor). In patients whose disease progressed after treatment with PD-1 inhibitors then 40% (2 out of 5) showed stable disease (SD) after treatment with EF-022.
EF-022 has also shown encouraging results in a compassionate use case. A patient with pulmonary metastatic sarcoma received weekly injections (100 ng/each injection) intramuscularly (IM) for one year. As a result, disease stabilization was achieved for 6 months. Thereafter, relapse accompanied with new lesions in the lungs occurred. At that stage, the patient received a combination therapy of it and the anti-PD-1 drug Keytruda which was administered by intravenous (IV) injection every three weeks. The combination was continued for an additional 6 months. This resulted in disease stabilization and complete disappearance of one of the lung metastases (FIGs. IB and 1C). Thus, the combination therapy was found to be more efficacious than either treatment alone.
Then a patient with oral cavity squamous cell carcinoma (SCC) who after failing SOC (chemotherapy and Keytruda) showed stable disease (SD) after treatment with EF-022. It was shown that it unexpectedly increased the number of cytotoxic T cells and macrophages in the tumour site, leading to disease stabilization despite the extremely high increase in PD-L1 expression on the tumour cells and/or adjacent cells during the EF-022 treatment course.
This shows the number of cells expressing PD-L1 from tumour biopsies collected from the patient prior to treatment (baseline) and after 57 days
It should be noted that high expression of PD-L1 on tumour cells and/or adjacent cells is typically linked with immune suppression and poor prognosis. Yet, treating this patient for four months resulted in disease stabilization and then tumour shrinkage. This result indicates that in spite of the high expression of PD-L1 EF-022 was capable of arresting tumour growth.
This shows staining of CD8+ T cells in biopsies collected from the same patient. They show a significant increase (115% compared to baseline) in the level of these