Anti CCL mAb to treat castration resistant prostate cancer

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R41CA214080-01
Agency Tracking Number: R41CA214080
Amount: $350,000.00
Phase: Phase I
Program: STTR
Solicitation Topic Code: 102
Solicitation Number: PA15-270
Timeline
Solicitation Year: 2015
Award Year: 2017
Award Start Date (Proposal Award Date): 2017-01-01
Award End Date (Contract End Date): 2018-12-31
Small Business Information
3393 RAES CREEK RD, Marietta, GA, 30008-5702
DUNS: 832442771
HUBZone Owned: N
Woman Owned: N
Socially and Economically Disadvantaged: N
Principal Investigator
 SHAILESH SINGH
 (404) 337-6012
 singshailesh@gmail.com
Business Contact
 JAMES LILLARD
Phone: (678) 697-5220
Email: james.lillard@jyanttech.com
Research Institution
 MOREHOUSE SCHOOL OF MEDICINE
 720 WESTVIEW DR SW
ATLANTA, GA, 30310-1495
 Nonprofit college or university
Abstract
Metastatic castration resistant prostate cancer CRPC PCa accounts for of PCa deaths and is associated with skeletal metastases CRPC affects patients differently making this disease difficult for physicians to provide standardized treatments with similar outcomes Docetaxel can prolong the overall survival in patients with metastatic CRPC but current therapies do not provide a cure Docetaxel non selectively targets rapidly dividing cell populations but also causes systemic toxicities CRPC cells have a relative slow growth rate Hence it is crucial to develop therapies to target less proliferative metastatic CRPC cells along with standard chemotherapies To address these issues investigators at Morehouse School of Medicine and JYANT Technologies Inc have identified a critical pathway that controls PCa cell growth metastasis and docetaxel response rates the CCL CCR axis Our recently published and exciting supportive data show that i CCR is highly expressed by PCa cells and tumors and mediates PCa progression ii CCL the sole ligand for CCR is elevated in prostate tumors and PCa patient serum iii bone marrow stromal cells of tumor bearing mice significantly produce CCL and iv blockade of the CCL CCR axis sensitizes PCa cells to docetaxel Importantly we show that our murine anti human CCL antibody candidate shrinks CRPC xenografts established in femurs of SCID mice In consideration of these findings JYANT Technologies seeks to develop a humanized anti human CCL monoclonal antibody CCL HuMAB for the treatment of CRPC To complete these objectives we will use clinically relevant mouse models of osteolytic and osteoblastic CRPC as well as docetaxel resistant xenografts to carryout the following aims Aim One will ascertain the immunogenicity using na ve B mice and the PK PD profile of CCL HuMAB in SCID mice bearing luciferase expressing osteolytic PC luc and osteoblastic C b luc xenografts in femurs Aim Two will determine the systemic and immune toxicity as well as the efficacy of CCL HuMAB to inhibit prostate tumor growth and docetaxel resistance in bone using SCID mice challenged in femurs with castration resistant PC luc and C b luc and or docetaxel resistant PC R luc and C bR luc PCa cell lines To date there is no cure for metastatic castration resistant prostate cancer CRPC PCa chemoresistance adverse drug events and variable response rates hinder the use of many drugs e g docetaxel to treat PCa Using clinically relevant metastatic CRPC models this study tests the utility of targeting the CCL CCR axis

* Information listed above is at the time of submission. *

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