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HaemaLogiX is engaged in three broad areas of research and development.


First, Research & Discovery involves discovering and developing new antibodies and CAR T cells.

Second, Preclinical testing includes testing antibody candidates in the lab to show that, for example, they bind to the intended target(s).

Third, Phases 1-3 are clinical trials, where safety and effectiveness (efficacy) are tested in stages in humans.

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PhIIb trial complete - data to be published soon

Dose optimisation trial opening soon

Phase IIb trial in 40 patients completed, dose optimisation trail opening soon

Indication: Multiple Myeloma

Phase III

Research & Discovery


Phase I

Phase II


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Our lead antibody, KappaMab, is in clinical trials to treat patients with kappa-type myeloma cells (i.e., kappa-restricted myeloma). In a first-in-human Phase I clinical trial, multiple myeloma patients were given a single intravenous infusion of the KappaMab antibody at increasing doses to assess safety. Following administration of KappaMab, there were no dose-limiting toxicities, and the maximum tolerated dose was not reached at the highest dose. Based on these findings and the observed activity of the antibody on myeloma disease, a dose level of 10 mg/kg of KappaMab was then explored in a multiple dose Phase IIa clinical trial. The antibody was shown to have disease responses and was well tolerated when given to patients as a weekly dose for 8 weeks.

As the antibody was well tolerated and Revlimid was shown to enhance the activity of KappaMab in vitro, a Phase IIb clinical trial in relapsed-refractory myeloma patients was initiated. This two-stage study evaluated the effects of the antibody alone in stage 1 and then in stage 2, in combination with Revlimid and dexamethasone. This clinical trial is completed and the results have been finalised for publication.


The statistical design for a monotherapy KappaMab dose optimisation study at 30mg/kg is now complete and the HaemaLogiX Scientific Advisory Board is in the final stages of the protocol review. It is anticipated that the higher dose of KappaMab  will not result in additional safety concerns and may increase the depth and duration of responses. Once safety of the higher dose has been established a KappaMab clinical trial in combination with Pomalidomide plus dexamethasone in patients who have failed standard of care treatment will be initiated. In addition, a clinical trial of KappaMab in combination with Revlimid is planned for patients who are given maintenance treatment after an autologous stem cell transplant.   

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LambdaMab candidate selection is ongoing


Lambda Myeloma Antigen (LMA) is another unique target that is found on lambda-type myeloma cells, occasional mononuclear cells in tonsillar tissue and secondary mucosal lymphoid tissue but not on normal B cells in the human body. We have proven the existence of LMA on myeloma cells and we have two human LambdaMab antibody candidates with different binding characteristics in development.


We will explore if the two antibody candidates are useful in different diseases such as multiple myeloma and AL amyloidosis (a form of myeloma which is predominantly lambda type). In AL Amyloidosis, deposits of amyloid are laid down most frequently in the heart and kidneys, which cause irreparable organ damage. Currently, these antibodies are being tested in vitro (in the lab) against human myeloma cell lines and myeloma and amyloidosis bone marrow samples.

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Proof of concept preclinical studies completed, trial to be initiated

Trial to be initiated soon


CAR T cell technology is a form of personalised medicine. To make CAR T cells, a cancer patient’s own T cells are collected, genetically modified in the laboratory, multiplied many times in culture to create billions of cells that are then infused back into the same patient. The cell surfaces of these modified T cells contain the special receptor (the Chimeric Antigen Receptor, or CAR), which expresses the KappaMab binding region that recognises Kappa Myeloma Antigen (KMA) on the surface of myeloma cells.


In vitro studies have shown that these KMA.CAR T cells recognise and specifically kill only cells with the KMA surface antigen--that is, only the myeloma cells. The manufacturing process for producing an individual myeloma patient’s CAR T cells is currently under evaluation.

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Three candidate 
constructs, purification & affinity testing is the next step


Bispecific antibodies are genetically engineered to combine 2 different antibodies, one that binds an antigen on the myeloma cell and the other that binds to and stimulates a T cell that will attack the myeloma cell. 


HaemaLogiX is in the early phase of developing a bispecific antibody using the KappaMab antibody to target KMA on myeloma cells and an immune cell engager to bind to a T cell, bringing the myeloma cell and the T cell together to kill the myeloma cell.

*LMA.CAR-T and LMA Bispecific are potential future additions to our pipeline
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Indication: AL Amyloidosis

Preclinical evaluation of use in AL amyloidosis is ongoing


Patients with Amyloid Light-chain (AL) Amyloidosis can suffer from congestive heart failure, kidney failure and nerve damage due to the amyloid deposits in these organs and tissues. Amyloid is an aggregate of fibrils that can be arranged in bundles or in felt-like mesh in stacked sheets. These fibrils are formed from fragments of either kappa or lambda light chains. The light chains are produced by the malignant plasma cells, B cells in the bone marrow.


KMab binds to kappa light chains and the KMA  target on the surface of the amyloidosis malignant B cells and has the potential to block the kappa light chains from depositing and causing organ damage. At the same time KMab has the ability to bind to KMA and kill the amyloid-producing cells.

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10B3 & 7F11

Preclinical evaluation of  use in AL amyloidosis is ongoing


Patients with Amyloid Light-chain (AL) Amyloidosis more often have lambda light chain than kappa light chain. AL Amyloidosis patients can suffer from congestive heart failure, kidney failure and nerve damage due to the amyloid deposits in these organs and tissues. 


Our LMabs bind to lambda light chains and the LMA target on the surface of the malignant B cells and have the potential to block the lambda light chains from depositing and causing organ damage. At the same time both LMab antibodies have the ability to bind to LMA and kill the amyloid producing cells.


Published Manuscripts


Poster Presentations

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