Partnerships
Let’s co-create to deliver cutting-edge solutions
We believe that combining forces will help us deliver innovative solutions at an accelerated pace.
Ichnos Glenmark Innovation invites collaboration with partners who share the same
belief and can complement our capabilities to propel forward innovations in cancer therapy.
We seek to collaborate through, both, out-licensing and in-licensing opportunities.
Partnerships for Oncology Pipeline
Ichnos Glenmark Innovation is committed to advancing its clinical-stage oncology portfolio. We would like to join hands with partners who can help us fast-track our mission of bringing innovative therapeutics to patients with hematologic cancers and solid tumors.
- Overview
- ISB 1342
- ISB 1442
- ISB 2001
- GRC 54276
Diversity of Immune Cell Engagement and Indications across Hematologic and Solid Tumors
ASSETS | DESCRIPTION | INDICATION |
---|---|---|
PRODUCTS |
PRECLINICAL | PHASE 1 | PHASE 2 | PHASE 3 |
---|---|---|---|
STATUS |
---|
ISB 1342
CD38 x CD3 BEAT® bispecific antibody
Multiple Myeloma T-ALL under consideration
AVAILABLE FOR LICENSING
PHASE 1
ORPHAN DRUG
ISB 1442
CD38 x CD47 BEAT®
bispecific antibody
Multiple Myeloma;
AML planned in 2024
PHASE 1
ORPHAN DRUG
ISB 2001
BCMA x CD38 x CD3
TREAT™ trispecific antibody
Multiple Myeloma
PHASE 1
ORPHAN DRUG
GRC 54276
Hematopoietic progenitor kinase 1 inhibitor
Solid Tumors
PHASE 1
PRODUCTS
COMPOUND
ISB 1342
TARGET
CD38 x CD3 BEAT® bispecific antibody
INDICATION
Multiple Myeloma T-ALL under consideration
PHASE
STATUS :
AVAILABLE FOR LICENSING
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
ISB 1442
TARGET
CD38 x CD47 BEAT® bispecific antibody
INDICATION
Multiple Myeloma; AML planned in 2024
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
ISB 2001
TARGET
BCMA x CD38 x CD3 TREATTM trispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
GRC 54276
TARGET
Hematopoietic progenitor kinase 1 inhibitor
INDICATION
Solid Tumors
PHASE
STATUS :
PHASE 1
ISB 1342 (CD38 x CD3) Bispecific Antibody: Potential
First-in-Class Therapy in Relapsed/Refractory Multiple Myeloma
- CD38 is expressed on the surface of multiple myeloma cells and is a validated target
- ISB 1342 is a bispecific antibody that redirects T cells to kill CD38-expressing tumor cells in MHC-antigen-independent manner
- ISB 1342 binds to a proprietary anti-CD38 epitope, which is different from that of daratumumab
ISB 1342 is designed to overcome:
– Daratumumab resistance by killing low CD38-expressing tumor cells
– Resistance to CDC and ADCC mediated by daratumumabISB 1342 was Granted Orphan Drug Designation for Multiple Myeloma by U.S. FDA
MHC: Major histocompatibility complex,
CDC: Complement-Dependent Cytotoxicity
ADCC: Antibody-Dependent Cell-mediated Cytotoxicity
ISB 1442 - Triple Mechanism of Tumor-Cell Killing
Enhanced ADCP, ADCC and CDC
- Dual binding to CD38 and CD47 epitopes, increasing avidity relative to daratumumab
- Two Fab regions drive binding to distinct CD38 epitopes that don’t compete functionally with daratumumab
- One arm blocks CD47-SIRPa binding on tumor cells to enhance ADCP
- Enhanced phagocytosis by blocking CD47 and increasing activation signaling through FcγR binding
- CD47 is over-expressed by hematologic tumors and associated with worse prognosis
- Reduced potential for antigen sink with lower-affinity Fab binding to CD47 expressed on healthy cells
- Potent ADCC, CDC and ADCP based on optimized affinity, architecture/avidity and enhanced
Fc function
- Optimized tolerability with low potential for adverse effects on red blood cells such as hemagglutination, platelet aggregation
- ISB 1442 was granted Orphan Drug Designation for Multiple Myeloma by the U.S. FDA
TREAT™: Trispecific Engagement by Antibodies based on the TCR, MHC: Major histocompatibility complex, CDC: Complement-Dependent Cytotoxicity ADCC: Antibody-Dependent Cell-mediated Cytotoxicity
ISB 2001 is first TREATTM Trispecific Antibody for
Relapsed/Refractory Multiple Myeloma
- BCMA and CD38 are expressed on the surface of multiple myeloma cells
and are clinically validated targets.
- ISB 2001 combines three proprietary Fab arms binding to CD3 on T-cells, and to BCMA and CD38 on myeloma cells.
- In vitro studies showed increased killing potency of tumor cells compared to all tested antibodies, including currently approved and investigational multiple myeloma therapies.
- In vivo studies in multiple myeloma models also show superior potency relative to antibodies for the treatment of multiple myeloma.
- ISB 2001 redirects CD3+ T lymphocytes to kill tumor cells expressing from low
to high levels of both BCMA and CD38. - With two different tumor-associated antigens, ISB 2001 is expected to be more resistant to antigen escape associated with treatment of MM patients
. - ISB 2001 was granted ODD by the U.S. FDA
GRC 54276 - HPK1 inhibitor known to activate APCs and T-cells
- GRC 54276 (HPK1 Inhibitor) is being developed as an orally administered IO-adjuvant treatment for patients with solid tumors. Hematopoietic progenitor kinase 1 (HPK1), is a negative regulator of T and B cell receptor signalling and an attractive therapeutic strategy for immuno-oncology based
treatment in cancers. - GRC 54276 is a novel, orally active HPK1 inhibitor that demonstrates excellent stand-alone efficacy and enhances current immunotherapy efficacy.
- In vitro, it has shown to potentiate cytokine release from DC and T-cells. It reverses Adenosine and PGE2 mediated immuno suppression.
- In vivo (murine colon cancer efficacy model) it inhibits tumor growth of 55% at the ED max of 30 mg/kg and of 75% in combination with CTLA4 antibody. Immune profile in GRC 54276 treated tumors showed increased IL-2 and IFNg levels along with cytotoxic T cells. It also inhibit pSLP76 (ser 376) with ED50 of 11.3 mg/kg.
- GRC 54276 is in development for advanced solid tumors
*Future clinical development will be advanced by a partner T-ALL: T-cell Acute Lymphoblastic Leukemia;
AML: Acute Myeloid Leukemia For collaborations, please contact us here.
Diversity of Immune Cell Engagement and Indications across Hematologic and Solid Tumors
ASSETS | DESCRIPTION | INDICATION |
---|---|---|
PRODUCTS |
PRECLINICAL | PHASE 1 | PHASE 2 | PHASE 3 |
---|---|---|---|
STATUS |
---|
ISB 1342
CD38 x CD3 BEAT® bispecific antibody
Multiple Myeloma T-ALL under consideration
AVAILABLE FOR LICENSING
PHASE 1
ORPHAN DRUG
ISB 1442
CD38 x CD47 BEAT®
bispecific antibody
Multiple Myeloma;
AML planned in 2024
PHASE 1
ORPHAN DRUG
ISB 2001
BCMA x CD38 x CD3
TREAT™ trispecific antibody
Multiple Myeloma
PHASE 1
ORPHAN DRUG
GRC 54276
Hematopoietic progenitor kinase 1 inhibitor
Solid Tumors
PHASE 1
PRODUCTS
COMPOUND
ISB 1342
TARGET
CD38 x CD3 BEAT® bispecific antibody
INDICATION
Multiple Myeloma T-ALL under consideration
PHASE
STATUS :
AVAILABLE FOR LICENSING
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
ISB 1442
TARGET
CD38 x CD47 BEAT® bispecific antibody
INDICATION
Multiple Myeloma; AML planned in 2024
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
ISB 2001
TARGET
BCMA x CD38 x CD3 TREATTM trispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
GRC 54276
TARGET
Hematopoietic progenitor kinase 1 inhibitor
INDICATION
Solid Tumors
PHASE
STATUS :
PHASE 1
ISB 1342 (CD38 x CD3) Bispecific Antibody: Potential
First-in-Class Therapy in Relapsed/Refractory Multiple Myeloma
- CD38 is expressed on the surface of multiple myeloma cells and is a validated target
- ISB 1342 is a bispecific antibody that redirects T cells to kill CD38-expressing tumor cells in MHC-antigen-independent manner
- ISB 1342 binds to a proprietary anti-CD38 epitope, which is different from that of daratumumab
ISB 1342 is designed to overcome:
– Daratumumab resistance by killing low CD38-expressing tumor cells
– Resistance to CDC and ADCC mediated by daratumumabISB 1342 was Granted Orphan Drug Designation for Multiple Myeloma by U.S. FDA
MHC: Major histocompatibility complex,
CDC: Complement-Dependent Cytotoxicity
ADCC: Antibody-Dependent Cell-mediated Cytotoxicity
ISB 1442 - Triple Mechanism of Tumor-Cell Killing
Enhanced ADCP, ADCC and CDC
- Dual binding to CD38 and CD47 epitopes, increasing avidity relative to daratumumab
- Two Fab regions drive binding to distinct CD38 epitopes that don’t compete functionally with daratumumab
- One arm blocks CD47-SIRPa binding on tumor cells to enhance ADCP
- Enhanced phagocytosis by blocking CD47 and increasing activation signaling through FcγR binding
- CD47 is over-expressed by hematologic tumors and associated with worse prognosis
- Reduced potential for antigen sink with lower-affinity Fab binding to CD47 expressed on healthy cells
- Potent ADCC, CDC and ADCP based on optimized affinity, architecture/avidity and enhanced
Fc function
- Optimized tolerability with low potential for adverse effects on red blood cells such as hemagglutination, platelet aggregation
- ISB 1442 was granted Orphan Drug Designation for Multiple Myeloma by the U.S. FDA
TREAT™: Trispecific Engagement by Antibodies based on the TCR, MHC: Major histocompatibility complex, CDC: Complement-Dependent Cytotoxicity ADCC: Antibody-Dependent Cell-mediated Cytotoxicity
ISB 2001 is first TREATTM Trispecific Antibody for
Relapsed/Refractory Multiple Myeloma
- BCMA and CD38 are expressed on the surface of multiple myeloma cells
and are clinically validated targets.
- ISB 2001 combines three proprietary Fab arms binding to CD3 on T-cells, and to BCMA and CD38 on myeloma cells.
- In vitro studies showed increased killing potency of tumor cells compared to all tested antibodies, including currently approved and investigational multiple myeloma therapies.
- In vivo studies in multiple myeloma models also show superior potency relative to antibodies for the treatment of multiple myeloma.
- ISB 2001 redirects CD3+ T lymphocytes to kill tumor cells expressing from low
to high levels of both BCMA and CD38. - With two different tumor-associated antigens, ISB 2001 is expected to be more resistant to antigen escape associated with treatment of MM patients
. - ISB 2001 was granted ODD by the U.S. FDA
GRC 54276 - HPK1 inhibitor known to activate APCs and T-cells
- GRC 54276 (HPK1 Inhibitor) is being developed as an orally administered IO-adjuvant treatment for patients with solid tumors. Hematopoietic progenitor kinase 1 (HPK1), is a negative regulator of T and B cell receptor signalling and an attractive therapeutic strategy for immuno-oncology based
treatment in cancers. - GRC 54276 is a novel, orally active HPK1 inhibitor that demonstrates excellent stand-alone efficacy and enhances current immunotherapy efficacy.
- In vitro, it has shown to potentiate cytokine release from DC and T-cells. It reverses Adenosine and PGE2 mediated immuno suppression.
- In vivo (murine colon cancer efficacy model) it inhibits tumor growth of 55% at the ED max of 30 mg/kg and of 75% in combination with CTLA4 antibody. Immune profile in GRC 54276 treated tumors showed increased IL-2 and IFNg levels along with cytotoxic T cells. It also inhibit pSLP76 (ser 376) with ED50 of 11.3 mg/kg.
- GRC 54276 is in development for advanced solid tumors
BEAT® Platform Partnerships
IGI is constantly striving towards advancement of the next wave of discovery-stage assets.
Our BEAT® platform enables deep exploration of the bi/multispecific design space to optimize drug candidates and unlock new biology including T-cell, NK cells, macrophage engagers.
The BEAT® Features include:
- Heavy chain pairing technology
- Heavy/light chain pairing technology using a common light chain
- Proprietary tools for selection of high-quality antibodies (phage and mammalian display)
- Effective target affinity and avidity maturation
- Efficient purification aided by differential binding to Protein A, 95% yield in a single purification step
- Flexible platform enables exploration of the full design space
- Fc function activity can be modulated (T-cell: silent; non T-cell: active or enhanced)
- Comprehensive screening capabilities enabling fast identification of leads with best functional activity and drug-like properties
Autoimmune Disease Partnerships
Ichnos Glenmark Innovation has out-licensed two assets that were developed to treat a range of autoimmune diseases with high unmet need.
ASSETS | DESCRIPTION | |
---|---|---|
PRODUCTS |
PRECLINICAL | PHASE 1 | PHASE 2 | PHASE 3 |
---|---|---|---|
Alliance Partner |
---|
Ready to join hands?
In-licensing
We are also open to explore any in-licensing opportunities.
Our scale and speed of clinical trials enable us to work with partners who are seeking solutions for an array of medical challenges. We are equipped to collaborate with them at various stages of product development, across the disease spectrum. Furthermore, with easy access to study participants in India and across the globe, we bring a unique advantage to our partners who endeavor to expedite the trials.
We seek partners who have
Differentiated assets in
hematology-oncology and
solid tumors
Innovative technologies
and clinical-stage assets
Aim to access the large
and growing market
in India