What distinguishes Kancera?

Kancera’s leading drug candidates work through a system that precisely controls cancer cells and immune cells, the so-called Fractalkine system. New discoveries by several independent research groups have shown that the Fractalkine system is of crucial importance for how difficult a cancer is to treat and how severe an inflammatory condition develops. Kancera works mainly with the clinical development of small molecules that block the Fractalkine system. Thus, Kancera has a unique opportunity to develop a new class of drugs for treatment that breaks down harmful acute inflammation and progressive cancer.

Kancera’s goal for this new class of drugs is to:

Protect the heart and kidneys in connection with a heart attack and acute kidney damage, by blocking the inflammatory cells while other parts of the immune system remain intact as protection against infection.

Attack treatment-resistant tumors by blocking the cancer cells’ ability to repair their DNA and thus resist chemotherapy and radiation, while surrounding healthy tissue is not affected to the same extent, which aids rehabilitation.

Small-molecule drugs of the class that Kancera develops have an important role in both current care and in the next generation of drug treatments that require increased efficacy and quality of life.

Fractalkine blockers against cancer and inflammation

Kancera is leading the development of new classes of drugs against treatment-resistant cancer and hyperinflammation. The company is currently focusing on the development of three drug candidates.

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Pharmaceutical Development

Kancera is leading the development of new classes of drugs against treatment-resistant cancer and hyperinflammation. The company is currently focusing on the development of two drug candidates:

Focus: Acute heart, kidney and lung damage that occurs due to vascular problems and resulting excessive inflammation, so-called hyperinflammation.

Status: Phase 2 clinical development.

Every year, about 500,000 people worldwide suffer from a major acute myocardial infarction. These patients undergo a vital treatment that opens and dilates the clogged vessel, and then a hyperinflammation can be triggered due to mechanisms that include activation of the fractalkine system. Hyperinflammation can aggravate heart damage and contribute to the severe prognosis, which carries the risk of death or other serious complications in one in four patients within five years of the heart attack. Negative effects of hyperinflammation include a deterioration in the function of the important small vessels that supply the heart muscle with oxygen and nutrition and a change in the shape and function of the heart, which together are closely linked to an increased risk of chronic heart failure.

In Kancera’s ongoing Phase IIa study with KAND567 in myocardial infarction patients, the fractalkine system is blocked with the aim of counteracting hyperinflammation, reducing heart damage and, in the long run, facilitating the return to a normal life.

Focus: Orphan indications with the capacity to break down resistance to cytostatics by blocking the ability of cancer cells to repair DNA.

Status: Clinical preparatory studies and production prior to phase Ia / IIa in the treatment of ovarian cancer.

Ovarian cancer affects more than 300,000 women worldwide each year. The disease is considered to be the most difficult-to-treat form of gynecological cancer and the need for long-term treatments is therefore great.

Kancera´s drug candidate KAND145 blocks the tumor cells´ ability to repair DNA, which may affect treatment-resistant tumors so that they become sensitive to chemotherapy again.

KAND145 thus has the potential to be a valuable addition to the treatment of difficult-to-treat cancer. Kancera is now conducting preclinical studies in preparition for the upcoming clinical evaluation of KAND145 against ovarian cancer.

Focus: Increase the effect of chemotherapy and radiation treatment of stage II and III rectal cancer to achieve complete recovery of the tumor, reduce the need for radical surgery and thus preserve intestinal function.

Status: Preclinical evaluation of the proportion of patients who can benefit from treatment and development of a product for local treatment of the tumor.

Colon cancer is the second most common cause of cancer-related mortality in the world and rectal cancer is the second most serious form. In stages II and III of rectal cancer, the tumor has advanced but not yet metastasized. The main clinical goal for the treatment of these patients is to increase the proportion who respond well to chemotherapy and radiation (about 30% respond positively to this treatment today) to prevent the spread and reduce the need for comprehensive surgery that destroys intestinal function. Kancera’s drug candidate KAND757 has in preclinical studies shown increased effect of chemotherapy and radiation and shown effective killing of isolated human tumor tissue. This effect profile of KAND757 is based on the drug candidate uniquely blocking the cancer’s metabolism, which disrupts the cancer’s ability to generate energy and building blocks for repair. Thus, KAND757 exhibits the properties that are sought after for the next generation of so-called “neo-adjuvants” that aim to strengthen the cancer-specific effect of chemotherapy and radiation and thus contribute to prolonging life and maintaining quality of life for patients with rectal cancer.

Other Projects

The following two exploratory research projects are being evaluated in collaboration with academic researchers with the aim of producing a basis for decisions to possibly take the next step in development through clinical preparatory studies. However, such studies require new funding.

  • Small molecule ROR inhibitors that reprogram the cancer cells so they destroy themselves. ROR inhibitors have been shown to work in the laboratory in disease models of mainly blood cancer.
  • Small molecule HDAC6 inhibitors that primarily aim to kill blood cancer cells (e.g. myeloma) by preventing the ability of cancer cells to spread and supporting the immune system’s ability to recognize and eliminate cancer cells.


Kancera’s strategy is to obtain strong patent protection and data protection for current and future drug candidates. The patent portfolio is global and covers the markets that are judged to be clinically and commercially most relevant for the products.

Preclinical Research Clinical Research
Medicinal Discovery Optimization of Drug Candidates Preparations for Clinical Studies* Clinical Phase I** Clinical Phase II*** Partner


– Hyperinflammation associated with myocardial infarction


– Hyperinflammation in kidneys


– Solid tumours (ovarian cancer)


– First in human


– Chronic lymphocytic leukemia


– Mantle cell lymphoma


– Colorectal cancer

The transparent fields illustrate ongoing funded projects

* Toxicologi & Production
** Safety, Tolerability & Drug Properties
*** Safety, Tolerability, Pharmakologi, Clinical Effect & Dosing

Scientific Publications


In a study with 480 heart attack patients, Kancera's partner Professor Ioakim Spyridopoulos and his research group have shown the potential for the Fractalkine blocker KAND567 to prolong life after an acute heart attack.

Spray L, Park C, Cormack S, Mohammed A, Panahi P, Boag S, Bennaceur K, Sopova K, Richardson G, Stangl VM, Rech L, Rainer PP, Ramos GC, Hofmann U, Stellos K, Spyridopoulos I.
The Fractalkine Receptor CX3CR1 Links Lymphocyte Kinetics in CMV-Seropositive Patients and Acute Myocardial Infarction With Adverse Left Ventricular Remodeling. Front Immunol. 2021 May 5;12:605857. doi: 10.3389/fimmu.2021.605857. PMID: 34046028; PMCID: PMC8147691.

Positive research results for Kancera's Fractalkine blockers may pave the way for new treatment for ovarian cancer

Lehto J, Huguet Ninou A, Chioureas D, Jonkers J, Gustafsson NMS.
Targeting CX3CR1 Suppresses the Fanconi Anemia DNA Repair Pathway and Synergizes with Platinum. Cancers (Basel). 2021 Mar 22;13(6):1442. doi: 10.3390/cancers13061442. PMID: 33810010; PMCID: PMC8004634.


In a comprehensive research study, the PFKFB3 inhibitor KAND757 has been shown to effectively kills tumor tissue from rectal cancer patients by selectively blocking metabolism.

De Oliveira T, Goldhardt T, Edelmann M, Rogge T, Rauch K, Kyuchukov ND, Menck K, Bleckmann A, Kalucka J, Khan S, Gaedcke J, Haubrock M, Beissbarth T, Bohnenberger H, Planque M, Fendt SM, Ackermann L, Ghadimi M, Conradi LC.
Effects of the Novel PFKFB3 Inhibitor KAN0438757 on Colorectal Cancer Cells and Its Systemic Toxicity Evaluation In Vivo. Cancers (Basel). 2021 Feb 28;13(5):1011. doi: 10.3390/cancers13051011. PMID: 33671096; PMCID: PMC7957803.

KAND757 renders cancer cells, including treatment-resistant cancer cells, sensitive to platinum drugs while preserving normal cells.

Ninou AH, Lehto J, Chioureas D, Stigsdotter H, Schelzig K, Åkerlund E, Gudoityte G, Joneborg U, Carlson J, Jonkers J, Seashore-Ludlow B, Gustafsson NMS.
PFKFB3 Inhibition Sensitizes DNA Crosslinking Chemotherapies by Suppressing Fanconi Anemia Repair. Cancers (Basel). 2021 Jul 18;13(14):3604. doi: 10.3390/cancers13143604. PMID: 34298817; PMCID: PMC8306909.

In preclinical models, KAN0438757 has demonstrated a potent anti-tumor effect.

Gustafsson NMS, Färnegårdh K, Bonagas N, Ninou AH, Groth P, Wiita E, Jönsson M, Hallberg K, Lehto J, Pennisi R, Martinsson J, Norström C, Hollers J, Schultz J, Andersson M, Markova N, Marttila P, Kim B, Norin M, Olin T, Helleday T.
Targeting PFKFB3 radiosensitizes cancer cells and suppresses homologous recombination. Nat Commun. 2018 Sep 24;9(1):3872. doi: 10.1038/s41467-018-06287-x. PMID: 30250201; PMCID: PMC6155239.


The ROR inhibitor KAN571 shows a good killing effect on cells from patients with the difficult-to-treat disease mantle cell lymphoma. The results also show that KAN571 increases the effect of other types of cancer drugs against MCL.

Ghaderi A, Zhong W, Okhovat MA, Aschan J, Svensson A, Sander B, Schultz J, Olin T, Österborg A, Hojjat-Farsangi M, Mellstedt H.
A ROR1 Small Molecule Inhibitor (KAN0441571C) Induced Significant Apoptosis of Mantle Cell Lymphoma (MCL) Cells. Pharmaceutics. 2022 Oct 20;14(10):2238. doi: 10.3390/pharmaceutics14102238. PMID: 36297673; PMCID: PMC9607197.

ROR and Bcl2 inhibitors have shown a positive effect in laboratory experiments, in which the combination of these substances has been shown to effectively destroy cells from small cell lung cancer.

Wang WZ, Shilo K, Amann JM, Shulman A, Hojjat-Farsangi M, Mellstedt H, Schultz J, Croce CM, Carbone DP.
Predicting ROR1/BCL2 combination targeted therapy of small cell carcinoma of the lung. Cell Death Dis. 2021 Jun 4;12(6):577. doi: 10.1038/s41419-021-03855-w. PMID: 34088900; PMCID: PMC8178315.

The ROR inhibitor KAND571 has been shown in studies to have the capacity to disrupt the treatment resistance of leukemia cells.

Ghaderi A, Okhovat MA, Wikanthi LSS, Svensson A, Palma M, Schultz J, Olin T, Österborg A, Mellstedt H, Hojjat-Farsangi M.
A ROR1 small molecule inhibitor (KAN0441571C) induced significant apoptosis of ibrutinib-resistant ROR1+ CLL cells. eJHeam, 2021, May, https://doi.org/10.1002/jha2.232

The ROR inhibitor KAND571 in combination with the drug venetoclax shows almost complete elimination of cells from the malignant tumor diffuse large cell B-cell lymphoma (DLBCL = Diffuse Large B-Cell Lymphoma).

Ghaderi A, Daneshmanesh AH, Moshfegh A, Kokhaei P, Vågberg J, Schultz J, Olin T, Harrysson S, Smedby KE, Drakos E, Rassidakis GZ, Österborg A, Hojjat-Farsangi M, Mellstedt H.
ROR1 Is Expressed in Diffuse Large B-Cell Lymphoma (DLBCL) and a Small Molecule Inhibitor of ROR1 (KAN0441571C) Induced Apoptosis of Lymphoma Cells. Biomedicines. 2020 Jun 23;8(6):170. doi: 10.3390/biomedicines8060170. PMID: 32586008; PMCID: PMC7344684.