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.
IGI 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
IGI 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 1442
- ISB 2001
- GRC 65327
Diversity of Immune Cell Engagement and Indications across Hematologic and Solid Tumors
| ASSETS | DESCRIPTION | INDICATION |
|---|---|---|
| PRODUCTS |
| PRECLINICAL | PHASE 1 | PHASE 2 | PHASE 3 |
|---|---|---|---|
| STATUS |
|---|
CD38 x CD47 BEAT®
bispecific antibody
Multiple Myeloma
PHASE 1
ORPHAN DRUG
BCMA x CD38 x CD3 TREAT ™ trispecific T-Cell Engager
Multiple Myeloma
PHASE 1
ORPHAN DRUG
GRC 65327
Cbl-b Inhibitor Small Molecule
Solid Tumors
PRE-CLINICAL
PRODUCTS
COMPOUND
ISB 1342
TARGET
CD38 x CD3 BEAT® bispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
TARGET
CD38 x CD47 BEAT® bispecific antibody
INDICATION
Multiple Myeloma; AML planned in 2024
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
TARGET
BCMA x CD38 x CD3 TREATTM trispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
GRC 65327
TARGET
Cbl-b Inhibitor Small Molecule
INDICATION
Solid Tumors
PHASE
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 65327 A Novel Small Molecule
Selective Oral Cbl-b Inhibitor Immunotherapeutics
- Selective, small molecule, orally available, Cbl-b inhibitor, phase I-ready for solid tumor indications.
- Demonstrated nM Cbl-b activity, >20-fold selectivity, potentiation of IL-2 and IFN-γ and T cells proliferation.
- Significant tumor growth inhibition as a monotherapy and in combination with anti-PD1, while also inducing durable complete responses associated with memory immune responses.
- In a 1-month GLP monkey toxicology study, an increased T cells activation and infiltration was observed in mesenteric lymph nodes (a tissue immune response) at very low exposures of AUC ~1500 ng.h/mL and above.
- IND submission to DCGI completed in October 2024
*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 |
|---|
CD38 x CD47 BEAT®
bispecific antibody
Multiple Myeloma
PHASE 1
ORPHAN DRUG
BCMA x CD38 x CD3 TREAT ™ trispecific T-Cell Engager
Multiple Myeloma
PHASE 1
ORPHAN DRUG
GRC 65327
Cbl-b Inhibitor Small Molecule
Solid Tumors
PRE-CLINICAL
PRODUCTS
COMPOUND
ISB 1342
TARGET
CD38 x CD3 BEAT® bispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
TARGET
CD38 x CD47 BEAT® bispecific antibody
INDICATION
Multiple Myeloma; AML planned in 2024
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
TARGET
BCMA x CD38 x CD3 TREATTM trispecific antibody
INDICATION
Multiple Myeloma
PHASE
STATUS :
PHASE 1 ORPHAN DRUG
PRODUCTS
COMPOUND
GRC 65327
TARGET
Cbl-b Inhibitor Small Molecule
INDICATION
Solid Tumors
PHASE
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 65327 A Novel Small Molecule
Selective Oral Cbl-b Inhibitor Immunotherapeutics
- Selective, small molecule, orally available, Cbl-b inhibitor, phase I-ready for solid tumor indications.
- Demonstrated nM Cbl-b activity, >20-fold selectivity, potentiation of IL-2 and IFN-γ and T cells proliferation.
- Significant tumor growth inhibition as a monotherapy and in combination with anti-PD1, while also inducing durable complete responses associated with memory immune responses.
- In a 1-month GLP monkey toxicology study, an increased T cells activation and infiltration was observed in mesenteric lymph nodes (a tissue immune response) at very low exposures of AUC ~1500 ng.h/mL and above.
- IND submission to DCGI completed in October 2024
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
IGI has out-licensed two assets that were developed to treat a range of autoimmune diseases with high unmet need.
Autoimmune Disease
PRODUCTS
Telazorlimab (and ISB 830-X8)
DESCRIPTION
OX40 antagonist
Monoclonal Antibody
Atopic Dermatitis*
Alliance Partner
$320 million for upfront payment, development, regulatory and sales milestone payments,
plus tiered royalties on global sales
STATUS
SUCCESSFUL
PHASE 2B*
Alliance Partner
$320 million for upfront payment, development, regulatory and sales milestone payments,
plus tiered royalties on global sales
STATUS
PRE-CLINICAL
Alliance Partner
€20.8 million for upfront payment. Plus development, regulatory and sales milestone payments,
and tiered royalties on global sales
| PRODUCTS | DESCRIPTION | |
|---|---|---|
| PRECLINICAL | PHASE 1 | PHASE 2 | PHASE 3 |
|---|---|---|---|
| STATUS |
|---|
Licensed to
$320 million for upfront payment, development, regulatory and sales milestone payments,
plus tiered royalties on global sales
Licensed to
€20.8 million for upfront payment. Plus development, regulatory and sales milestone payments,
and tiered royalties on global sales
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