Type C Viral Hepatitis (closed)
IPH 1101 was tested in a Phase IIa clinical trial in HCV patients. Results of this trial were reported in June 2009 and were presented at the AFEF (Association Française pour l'étude du foie) and the AASLD (American Association for the Study of Liver Diseases) meetings in September and November 2009 respectively.
Phase II trial in Type C Viral Hepatitis (IPH 1101-203)
IPH 1101-203 was a multicenter, open label Phase IIa clinical trial designed to evaluate the effect on the viral load of IPH 1101 treatment with and without IL-2, as well as its tolerance and pharmacodynamics in chronically infected HCV patients who were either treatment naïve or had relapsed after one course of standard of care treatment.
The rationale of this trial was based on the known role of γδ T cells in anti-infectious immunity in general and in stimulating the production of certain cytokines in particular.
The primary efficacy endpoint of the trial was a decrease in the viral load of at least 0.5 log10 in at least 6 patients out of 13 evaluable patients in each arm.
The protocol called for the treatment of 26 patients (divided into 2 groups receiving IPH 1101 (750 mg/m²) with and without IL-2 (2 MIU) respectively) for two treatment cycles three weeks apart. 28 patients were included in the trial and evaluable for safety. 25 patients were evaluable for efficacy.
In Arm A, 5 out of the 13 (38%) evaluable patients showed a viral load decrease of at least 0.50 log10, with a median decrease of -0.69 log10 (+/-0.15). In Arm B, 7 patients out of 12 evaluable patients (58%) showed a viral load decrease of 0.50 log10 or more. The median decrease of responders in Arm B was -0.65 log10 (+/-0.13).
The viral load decrease after injection was rapid and lasted for up to three days. Ten of the 19 genotype 1 HCV patients and 2 out of the 3 genotype 4 HCV patients (the two most difficult-to-treat genotypes) had viral load decreases of more than 0.5 log10.
The viral load decrease correlated with biomarkers of immune activation, such as cytokine production, thus confirming the mode of action of γδ T cell stimulation on viral load decrease.
The tolerance was very good in this trial, with no serious adverse events reported.
Abstracts fully describing data and results of this trial were submitted to forthcoming international medical congresses.
Read the complete press release and download the slideshow presented during the conference call.
View posters presented at AASLD's 60th Annual Meeting (American Association for the Study of Liver Diseases) in Boston, MA, USA Oct 30 - Nov 3 2009
About type C chronic hepatitis
According to data from the World Health Organization (WHO), 170 million people may be chronically infected by HCV worldwide. There are probably about 3 or 4 million new cases of hepatitis C per year (Source: UNAIDS and WHO, 2005). Hepatitis C is known to be a major cause of cirrhosis and primary liver cancer (hepatocellular carcinoma). Furthermore, decompensated HCV-related cirrhosis is the leading cause of liver transplantation in Europe (source: Direction Générale de la Santé, France).
The standard treatment is based on a combination of interferon-α and ribavirin - both of which are aimed at blocking viral replication. This combination provides long-lasting control of the disease and prevents complications in about 50% of genotype 1 and 4 patients and about 80% of genotype 2 and 3 patients. Moreover, the length of the course of treatment (6 to 12 months) and the presence of side effects mean that only the most active forms of hepatitis C are treated.