Cidara is a clinical-stage biotechnology company focused on developing new anti-infectives that have the potential to transform the standard of care and save or improve patients’ lives. The company is currently advancing its novel echinocandin antifungal, CD101 IV, through Phase 2 and developing CD201, its bispecific antimicrobial immunotherapy, for the treatment of multi-drug resistant Gram-negative bacterial infections. CD101 IV has enhanced potency and is the only once-weekly therapy intended for the treatment and prevention of life-threatening invasive fungal infections. CD201 is the first drug candidate selected from Cidara’s novel Cloudbreak™ platform, the first immunotherapy discovery platform designed specifically to create compounds that direct a patient’s immune cells to attack and eliminate bacterial, fungal or viral pathogens. Cidara is headquartered in San Diego, California.
We are developing a balanced pipeline of product and development candidates with a focus on serious fungal and bacterial infections. Our lead product candidate, CD101 IV, is a novel echinocandin antifungal with enhanced potency and the only once-weekly therapy intended for the treatment and prevention of life-threatening invasive fungal infections. In addition, we have created our proprietary Cloudbreak immunotherapy platform to generate new development candidates that will expand and diversify our pipeline. View our pipeline >>
CD101 IV is a novel molecule in the echinocandin class of antifungals. We are initially developing CD101 IV for the treatment of systemic Candida infections. These infections include candidemia and related cases of invasive candidiasis, fungal infections associated with high mortality rates. The current treatment alternatives for systemic fungal infections, including polyenes, azoles, and currently approved echinocandins, have limitations that may be addressed by novel antifungals. Despite these limitations, annual sales for systemic antifungals are approximately $4.0 billion dollars globally.
CD101 IV exhibits a high exposure early in the course of infection and prolonged half-life which, in contrast to all other echinocandins, allows for once-weekly front-loaded IV therapy and convenient outpatient dosing. We believe that this pharmacokinetic profile may overcome the limitations of the current standard of care by:
- Allowing single-agent treatment in both inpatient and outpatient settings
- Facilitating shorter and less costly hospital stays
- Offering the potential ability to treat less-susceptible pathogens and enhance tissue penetration at the site of infection
- Providing more convenient outpatient echinocandin treatment and prophylaxis regimens
- Improving compliance for outpatients
We have completed two Phase 1 clinical trials for CD101 IV: a single ascending dose trial (SAD) and a multiple ascending dose (MAD) trial. We are currently conducting an international Phase 2 clinical trial in candidemia called STRIVE. We expect results from this trial in the second half of 2017. Learn more about CD101 IV >>
Cloudbreak™ Immunotherapy Platform
Our proprietary Cloudbreak immunotherapy discovery platform has the potential to do for infectious disease what immunotherapy has done for cancer. Cloudbreak is a fundamentally new approach for the treatment of infectious disease which redirects the immune system to destroy fungal, bacterial and viral pathogens.
The design of the Cloudbreak immunotherapy platform recognizes that most infectious disease is due to a temporary deficiency in the function of the immune system. Our Cloudbreak candidates are designed to address this deficiency by recruiting components of the patient’s immune system to the site of infection. Cloudbreak supports the engineering of bi-specific agents that target the pathogen and prime the immune system to generate a more effective anti-infective response.
We are developing initial Cloudbreak candidates for the treatment of serious gram-negative bacterial infections. Learn more about the Cloudbreak Platform >>
Each Cloudbreak candidate has two molecules that are joined by a chemical linker: a targeting moiety (TM) that recognizes a cell surface target and an effector moiety (EM) that is recognized by the immune system. The coupling of the TM to the EM results in a bispecific molecule that can direct the immune system specifically to the targeted pathogen.