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Category Archives: Stem Cell Therapy

Later-Generation Cellular Therapies Look Promising in Hematologic Malignancies – Targeted Oncology

Currently approved CAR T-cell products for hematologic malignancies, all of which are indicated for aggressive, advanced, or relapsed/refractory (R/R) disease, include axicabtagene ciloleucel (axicel; Yescarta) for diffuse large B-cell lymphoma (DLBCL), other B-cell lymphomas, and follicular lymphoma (FL); tisagenlecleucel (Kymriah) for adults with DLBCL and young adults with B-cell precursor acute lymphoblastic leukemia (ALL); lisocabtagene maraleucel (liso-cel; Breyanzi) for DLBCL, high-grade B-cell lymphomas, and FL; brexucabtagene autoleucel (Tecartus) for mantle cell lymphoma; and idecabtagene vicleucel (Abecma) for multiple myeloma (MM).4-8

Mehdi Hamadani, MD, a professor of internal medicine at the Medical College of Wisconsin and director of the Adult Blood and Marrow Transplant Program at Clinical Cancer Center at Froedtert Hospital in Milwaukee, calls CAR T cells a very relevant therapeutic tool for lymphoma treatment.

There are obvious advantages of an autologous product. Your immune system is not going to reject an autologous blood product. Its going to be curative for some patients, and the toxicity profile is generally manageable. Most centers have enough experience to work with these toxicity signals, Hamadani said.

Toxicities include potentially life-threatening cytokine release syndrome (CRS) and neurologic toxicities4-8 and hematologic toxicities, including hemophagocytic lymphohistiocytosis/macrophage activation syndrome and cytopenia.8 Other shortfalls include limited antitumor activity and antigen escape (loss or downregulation of target antigen expression).1

Axi-cel, tisagenlecleucel, liso-cel, and brexucabtagene autoleucel are all anti-CD19 CAR T-cell therapies.4-7 Antigen escape causes CD19-negative relapse in approximately 30% of patients with lymphoma treated with these therapies, Hamadani said, rendering ineffective other CD19-directed therapies recently approved for aggressive lymphomas that might have been used for subsequent treatment (FIGURE1).

There are also logistical challenges. It takes time to collect patient cells, ship them to the manufacturing facility, generate the CAR T cells, and ship them back.

The turnaround between sending the product and getting the product back would be 3 to 5 weeks, depending on the commercial product. Some patients with lymphoma can wait 3 to 5 weeks. Some cant. Some patients can have disease progression or even death while waiting for the product to come back, Hamadani said, adding that complete manufacturing failures occur up to 10% of the time.

Sometimes the product does not meet prespecified FDA quality-control measures. Those CAR T cells are called out-of-spec products.

Other cellular therapies in development for hematologic malignancies may help address limitations of the current CAR T-cell therapies, said Jason Westin, MD, MS, director of Lymphoma Clinical Research, Department of Lymphoma/Myeloma, at The University of Texas MD Anderson Cancer Center in Houston.

There are many different types of next- generation cell therapies, but they share certain properties, Westin said. They generally have a faster production time, result in increased cell fitness, and have lower risk for toxicities, especially longer term, in comparison with the existing generation of therapies. Some of the most innovative approaches may result in autologous cell therapies that are delivered in near off-the-shelf timelines, which may [avoid] the risk from an allogeneic product and have greater persistence.

Idecabtagene, which targets B-cell maturation antigen (BCMA), is the only approved CAR T-cell product not targeting CD19.8 Hematologic malignancies that do not express CD19 and CD19-negative relapse in patients treated with CD19 CAR T cells could be addressed by targeting different antigens.

A CAR T-cell therapy directed at an alternative B-cell antigen, CD22, is in a phase 1 trial for B-cell ALL treatment (NCT02315612). Recently reported results showed that, of 208 patients, 62% had received a prior CD19 CAR T-cell treatment and 88% had received any prior CD19-targeted therapy; more than half had CD19-negative disease. CD4/ CD8 T-cell selection was used to enhance CAR T-cell manufacturing feasibility and reduce product variability. However, this resulted in increased inflammatory toxicities, requiring dose de- escalation. Nevertheless, the complete remission rate was 70%, supporting further development.9

Another CAR T-cell product in development targets CD33 and is being tested in a phase 1/2 trial (NCT03971799) recruiting children and young adults with acute myeloid leukemia.

Most CAR T-cell therapies in clinical trials contain only 1 costimulatory domain. MB-106, a fully human, third-generation, CD20- directed CAR T-cell product with 2 costimulatory domains is in an ongoing trial (NCT03277729) for B-cell non-Hodgkin lymphoma (NHL) and chronic lymphocytic leukemia (CLL). Initial lack of response has been ameliorated by manufacturing changes that included combined culture of CD4- and CD8-positive cells. Investigators have reported a 93% overall response rate (ORR) and a 67% complete response (CR) rate. This has been observed at particularly higher dose levels, which are also associated with faster CAR T-cell expansion; no relapses have been observed in patients with CRs. Use in combination or in sequence with a CD19 CAR T therapy has been proposed.10,11

Another strategy to counter antigen escape is to target 2 or more antigens.1 Multitargeting has been proposed to address CD19- negative and CD22-dim (diminished expression) relapses in ALL.2 One such bispecific CD19/CD22 CAR T-cell product is in a phase 1 trial in relapsed/refractory (R/R) B-cell ALL (NCT03185494).12 All 6 patients treated in this small trial experienced CRs, although 3 experienced relapse within 3 to 10 months. Only 1 relapse was due to antigen escape (CD19-negative/CD22-dim); the other 2 relapses were associated with decreased CAR T-cell persistence. Three of the 6 patients have an ongoing response, and toxicity has been manageable.12

A novel CAR molecule targeting both CD19 and CD22 is in ongoing phase 1 studies in R/R B-cell malignancies: 1 for adults (NCT03233854) and 1 for children and young adults (NCT03241940). Autolus Therapeutics has multiple CAR T products in development, including a CD19/CD22 product (AUTO3) investigated in AMELIA (NCT03289455), a completed phase 1/2 trial in B-cell ALL.13 In the ongoing ALEXANDER study (NCT03287817) of this bicistronic CAR T product in R/R DLBCL, the antiPD-1 immunotherapy pembrolizumab (Keytruda) is being added to AUTO3 treatment to reduce the likelihood of relapse.14

A bispecific anti-CD20, anti-CD19 CAR T product (LV20.19 CAR T cells) is in a phase 1 trial in patients with R/R B-cell malignancies (NHL and CLL; NCT03019055). This product is manufactured on site in a local stem cell processing laboratory, which allows prompt infusion of fresh, noncryopreserved CAR T cells. In the trial, the 28-day overall response rate was 82% (18 of 22 patients), with 64% CRs. The median overall survival was 20.3 months. There was no association between clinical responses and baseline CD19 or CD20 expression in tumors. CD19 antigen escape did not appear to underlie lack of response; loss of CD19 expression was not observed in patients who experienced relapse or treatment failure. Treatment of patients who previously received unsuccessful CD19 CAR T-cell therapy remains a challenge; of 5 such patients in this trial, only 1 achieved adequate CAR T-cell expansion and a CR. The LV20.19 CAR T cells contain the same murine anti-CD19 domain as the commercial CD19 CAR T-cell products those 5 patients previously had received, suggesting that prior exposure led to immune-mediated rejection of the murine portion, representing an obstacle to retreatment.15 Long-term follow-up (NCT03375619) continues.

Another type of adoptive T-cell therapy, TCR-engineered T-cell therapy, uses genetically modified T cells with a TCR that specifically binds to a tumor-associated antigen. Unlike CAR T cells, TCR T cells interact with a peptide antigen presented by major histocompatibility complex (MHC), also called human leukocyte antigen (HLA), making them more sensitive than CAR T cells and more effective in some contexts, particularly for treating solid tumors.16,17

A major advantage of TCR T cells over CAR T cells is that target antigens are not limited to cell surface proteins; TCR T cells can also bind intracellular proteins digested into peptides and presented by MHC. Additionally, the risk of CRS is reduced. Advantages of CAR T cells include their MHC/HLA independence. One barrier to TCR T-cell therapy is identifying targets that are sufficiently cancer specific to avoid off-target toxicities. TCR T-cell products in development that target a single antigen are subject to antigen escape in much the same way that single-target CAR T cells are. However, targeting antigens essential to maintaining the malignant phenotype, such as leukemia- initiating fusions, should overcome this barrier, as would the infusion of more than 1 TCR T-cell product or a single product that expresses multiple TCRs.17 Ongoing trials of TCR T-cell therapies in hematologic malignancies are summarized in the TABLE.

Natural killer (NK) cells are also being exploited in cellular therapies for hematologic malignancies. NK cells are lymphoid cells that play a role in the innate immune response to infectious agents and malignant cells. Unlike T cells, they do not need prior antigen exposure or MHC expression to kill transformed cells. Normal cells are spared because NK cells recognize critical self- antigens expressed on them.3

Sources of NK cells can be autologous or allogeneic, such as donor peripheral blood, umbilical cord blood, and stem cells, including induced pluripotent stem cells. Though considered less prone than other allogeneic cells to both graft-vs-host disease (GVHD) and host-vs-graft rejection, NK cells may be susceptible to immunosuppression by the tumor microenvironment. Because they occur in small numbers, NK cells need cytokine support to survive more than 1 to 2 weeks, and they often require ex vivo expansion and activation. Although repeated infusions of expanded donor NK cells may address the short life span, patients with R/R acute leukemias may not be able to wait for expansion.3,18

NK cells derived from induced pluripotent stem cells can be readily expanded, but as immature cells they may lack some killing function. Cell linederived NK cells have malignant potential and require irradiation. The creation of universal-donor, allogeneic NK cell banks may overcome some limitations with the option to provide educatable CAR NK cells for off-the-shelf therapy.3,18

CAR NK cells in trials for B-cell leukemias and lymphomas target CD19; BCMA is a target of CAR NK cells designed to treat MM. In a phase 1/2 study of R/R B-cell hematologic malignancies (NCT03056339), CD19-directed CAR NK cells derived from cord blood and engineered with a suicide gene safety switch produced responses in 8 of 11 patients. The NK cells were expanded ex vivo and were HLA mismatched with the recipient. Neither GVHD nor CRS occurred in any patient.3,19 Although these CAR NK cells were transduced using a retroviral vector,19 nonviral strategies to genetically modify NK cells using electroporation or transposons and CRISPR/Cas9 have led to increased efficiency and stable genomic insertion. Other CAR NK cell therapies in development for hematologic malignancies have CD33, CD20, CD38, CD123, CLL1, and FLT3 as single targets; dual-targeted products are directed to CD19/CD22.18

Other allogeneic products in development can address the limitations of turnaround time and manufacturing failures associated with current autologous CAR T-cell therapies. The allogeneic platform gives you the ability, in theory, [to] readily get the product, but for an allogeneic CAR you still have to check donor-specific antibodies in the patient, because if the patient has premade antibodies against the CAR, they will reject it. In addition, they may cause GVHD, as in an allogeneic transplant, Hamadani said.

ALLO-501A, an allogeneic anti-CD19 CAR T-cell therapy, is being tested in patients with R/R large B-cell lymphoma in the ongoing ALPHA-2 trial (NCT04416984). Proprietary gene editing technology was used to disrupt TRAC, a gene that encodes part of the TCR; without functioning TCRs, the infused CAR T cells cannot recognize and attack allogeneic antigens, which should eliminate GVHD. Similarly, the CD52 gene was knocked out via editing to allow the addition of ALLO647, a humanized anti-CD52 monoclonal antibody, to the lymphodepletion regimen to selectively deplete CD52-positive host T cells while preventing host rejection of the CD52-negative CAR T cells, enabling their expansion and persistence.20 Although the ALPHA-2 results were from a small cohort, they showed that ALLO-501As efficacy mirrored that of ALLO-501, a previous iteration containing rituximab recognition domains, in the ALPHA trial of patients with R/R NHL (NCT03939026). Additionally, ALLO-501A therapy with ALLO-647 lymphodepletion was well tolerated, with no GVHD, and redosing at disease progression was safe and may provide clinical benefit.20

PBCAR0191, another off-the-shelf, allogeneic CD19-targeting CAR T-cell therapy, is in an ongoing early-phase trial in patients with R/R NHL and B-cell ALL (NCT03666000). The trial is comparing the standard lymphodepletion regimen to an enhanced one with extended fludarabine and higher-dose cyclophosphamide. The results in the R/R NHL cohort favored enhanced lymphodepletion, with 50-fold greater peak CAR T-cell expansion and deeper, more durable clinical responses, including a higher CR rate.21

More data are needed to demonstrate the utility of the newer cellular therapy platforms, whether they be dual- targeting, third-generation, or off-the-shelf allogeneic products.

Cost is an issue that often goes unmentioned. Cost will become an increasingly important barrier for cellular therapy to be deployed at scale and potentially could be a reason to choose one approach over another if efficacy is similar, Westin said.

Hamadani agreed that cost is a major concern. People keep saying, Our CAR is going to be cheaper, and so far every single CAR that gets approved is more expensive than the last one, and when they see that the next is more expensive, they raise their price, he said. That is what happened with liso-cel. When lisocel [was] approved, it was more expensive than axi-cel, and axi-cel recently increased their price to match liso-cel. Allogene promises that its AlloCAR T therapies are going to be cheaper.

Other unmet needs include more effective cell therapies that provide more durable remissions for more patients.

Hamadani said he sees durable remission in approximately 40% of patients receiving CAR T-cell therapy, meaning that 60% will experience a relapse. More effective cellular therapy platforms are needed, safer platforms are needed, cheaper platforms are needed, Hamadani said.

The cell therapy field for patients with lymphoma is moving very fast, potentially with CAR T cells becoming a new standard of care for patients with first relapse of aggressive lymphomas, Westin said. Cell therapy may not be right for every patient with lymphoma, but it is a powerful new weapon that sets the example for the potential for cellular therapy against all cancers as we break down more barriers.

References:

1. Sterner RC, Sterner RM. CAR-T cell therapy: current limitations and potential strategies. Blood Cancer J. 2021;11:69. doi:10.1038/s41408-021-00459-7

2. Gill S, Brudno JN. CAR T-cell therapy in hematologic malignancies: clinical role, toxicity, and unanswered questions. Am Soc Clin Oncol Educ Book. 2021;41:1-20. doi:10.1200/ EDBK_320085

3. Basar R, Daher M, Rezvani K. Next-generation cell therapies: the emerging role of CAR-NK cells. Blood Advances. 2020;2020(1):570-578. doi:10.1182/hematology.2020002547

4. Yescarta. Prescribing information. Kite Pharma; 2021. Accessed July 28, 2021. https://bit.ly/3i9Lq8z

5. Kymriah. Prescribing information. Novartis; 2021. Accessed July 28, 2021. https://bit.ly/2TII8Qc

6. Breyanzi. Prescribing information. Juno Therapeutics; 2021. Accessed July 28, 2021. https://bit.ly/2WqTM33

7. Tecartus. Prescribing information. Kite Pharma; 2021. Accessed July 28, 2021. https://bit.ly/3yaLOJz

8. Abecma. Prescribing information. Celgene; 2021. Accessed July 28, 2021. https://bit.ly/2WAz9lj

9. Shah NN, Highfill SL, Shalabi H, et al. CD4/CD8 T-cell selection affects chimeric antigen receptor (CAR) T-cell potency and toxicity: updated results from a phase I anti-CD22 CAR T-cell trial. J Clin Oncol. 2020;38(17):1938-1950. doi:10.1200/JCO.19.03279

10. Shadman M, Yeung C, Redman MW, et al. Third generation CD20 targeted CAR T-cell therapy (MB-106) for treatment of patients with relapsed/refractory B-cell non-Hodgkin lymphoma. Blood. 2020;136(suppl 1):38-39. doi:10.1182/ blood-2020-136440

11. Shadman M, Yeung C, Redman M, et al. Immunotherapy using a 3rd generation CD20 targeted CAR T-cell (MB-106) for treatment of B-cell non-Hodgkin lymphoma (B-NHL) and chronic lymphocytic leukemia (CLL). European Hematology Association 2021 Congress; June 9-17, 2021; virtual. Abstract EP731. Accessed July 28, 2021. https://bit.ly/3ycf9mQ

12. Dai H, Wu Z, Jia H, et al. Bispecific CAR-T cells targeting both CD19 and CD22 for therapy of adults with relapsed or refractory B cell acute lymphoblastic leukemia. J Hematol Oncol. 2020;13(1):30. doi:10.1186/s13045-020-00856-8

13. Autolus. Broad pipeline of clinical programs. Accessed July 28, 2021. https://bit.ly/2Wnhygi

14. Ramakrishnan A, Ardeshna KM, Batlevi CL, et al. Phase 1 Alexander study of AUTO3, the first CD19/22 dual targeting CAR T cell therapy, with pembrolizumab in patients with relapsed/ refractory (rr) DLBCL. American Society of Hematology 2020 Annual Meeting. Accessed July 28, 2021. https://bit.ly/3i7BwnR

15. Shah NN, Johnson BD, Schneider D, et al. Bispecific anti-CD20, anti-CD19 CAR T cells for relapsed B cell malignancies: a phase 1 dose escalation and expansion trial. Nat Med. 2020;26(10):1569-1575. doi:10.1038/s41591-020-1081-3

16. Zhang J, Wang L. The emerging world of TCR-T cell trials against cancer: a systematic review. Technol Cancer Res Treat. 2019;18:1-13. doi:10.1177/1533033819831068

17. Biernacki MA, Brault M, Bleakley M. TCR-based immunotherapy for hematologic malignancies. Cancer J. 2019;25(3):179190. doi:10.1097/PPO.0000000000000378 1

8. Lamb MG, Rangarajan HG, Tullius BP, Lee DA. Natural killer cell therapy for hematologic malignancies: successes, challenges, and the future. Stem Cell Res Ther. 2021;12(1):211. doi:10.1186/s13287-021-02277-x

19. Liu E, Marin D, Banerjee P, et al. Use of CAR-transduced natural killer cells in CD19-positive lymphoid tumors. N Engl J Med. 2020;382(6):545-553. doi:10.1056/NEJMoa1910607

20. Locke FL, Malik S, Tees MT, et al. First-in-human data of ALLO-501A, an allogeneic chimeric antigen receptor (CAR) T-cell therapy and ALLO-647 in relapsed/refractory large B-cell lymphoma (RR LBCL): ALPHA2 study. J Clin Oncol. 2021;39(suppl 15):2529. doi:10.1200/JCO.2021.39.15_suppl.2529

21. Shah B, Jacobson CA, Solomon S, et al. Preliminary safety and efficacy of PBCAR0191, an allogeneic, off-theshelf CD19-targeting CAR-T product, in relapsed/refractory (rr) CD19+ NHL. J Clin Oncol. 2021;39(suppl 15):7516. doi:10.1200/JCO.2021.39.15_suppl.7516

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Later-Generation Cellular Therapies Look Promising in Hematologic Malignancies - Targeted Oncology

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Therapeutic Solutions International Reports Superior Neurogenesis Induction in Animal Model of Viral Induced Cognitive Dysfunction Compared to other…

ELK CITY, Idaho, Aug. 11, 2021 /PRNewswire/ --Therapeutic Solutions International, Inc., (OTC Markets: TSOI), reported today new data and a patent filing describing the superior ability of JadiCell adult stem cells to other stem cell types in terms of stimulating production of new brain cells in an animal model of inflammation. The process of producing new brain cells is termed "neurogenesis" and is an active area of research for the Company.

"We saw that increasing doses of double stranded RNA, which mimics viral induced inflammation, was associated with decreased neurogenesis, which is to be expected. Shockingly, out of the stem cells tested, only the JadiCells were capable of stimulating neurogenesis under conditions of inflammation" stated Dr. James Veltmeyer, Chief Medical Officer of the Company. "These data suggest the possibility that JadiCells may be useful not only for patients with acute COVID-19, which we will test in our upcoming clinical trial, but may also have the potential to fight the long-term consequence of this infection."

"We are eager to explore collaborations with other neurological companies. One interesting thing about the filed patent was the embodiment of combining JadiCells with various existing drugs such as oxytocin, human chorionic growth hormone, and SSRIs" said Famela Ramos, Vice President of Business Development for the Company.

In previous studies the Company has demonstrated the superior activity of JadiCell to other types of stem cells including bone marrow, adipose, cord blood, and placenta. Furthermore, the JadiCell was shown to be 100% effective in saving the lives of COVID-19 patients under the age of 85 in a double-blind placebo controlled clinical trial with patients in the ICU on a ventilator. In patients over the age of 85 the survival rate was 91%1.

"Given we are getting closer to starting our Phase I/II CTE2 and our Phase III COVID trial, the validation that our cells are more potent than other adult stem cells for the brain is very promising" said Timothy Dixon, President and CEO of the Company and co-inventor. "We are enthusiastic about the success of the JadiCells because of the following characteristics: a) long history of safety data; b) what appears to be superior efficacy data as compared to other stem cells in preclinical models; c) low cost of production; and d) promising human data."

About Therapeutic Solutions International, Inc.Therapeutic Solutions International is focused on immune modulation for the treatment of several specific diseases. The Company's corporate website is http://www.therapeuticsolutionsint.com, and our public forum is https://board.therapeuticsolutionsint.com/

1Therapeutic Solutions International Receives FDA Clearance to Initiate Phase III Pivotal Registration Trial for JadiCell Universal Donor COVID-19 Therapy2 Therapeutic Solutions International Completes FDA Requested Studies to Initiate JadiCell Chronic Traumatic Encephalopathy (CTE) Clinical Trial

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Therapeutic Solutions International Reports Superior Neurogenesis Induction in Animal Model of Viral Induced Cognitive Dysfunction Compared to other...

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Treatment of AML in Older Patients Almost At ‘The Holy Grail’ – Curetoday.com

Recent drug approvals in the acute myeloid leukemia (AML) space have allowed older patients with the disease to continue receiving less intensive therapies than their younger counterparts, while also providing them with improved outcomes.

Were almost at the holy grail where (we) have lower intensity therapy thats well tolerated, but that the response rates are higher, said Dr. Tapan Kadia, an associate professor in the department of leukemia at The University of Texas MD Anderson Cancer Center in Houston, in an interview with CURE. Theyre not reaching (the 85% seen) with intensive chemotherapy, but (theyre) much better.

Kadia recently presented on the topic of treating older patients with AML during CUREs Educated Patient Leukemia Summit and highlighted how its vastly different than treating younger, and more fit patients.

He explained how the incidence of AML increases as a person gets older and that 60% of people who receive a diagnosis are aged older than 60 years.

Because more than half of the patient population with AML is aged older than 60 years, Kadia stressed that treatment approaches should be individualized for each patient. And, he said, factors such as their comorbidities, age, ability to tolerate chemotherapy and whether they could be candidate for a stem cell or bone marrow transplant in the future should play a role in selecting which treatment option they receive.

The major point to get across (is) to characterize a leukemia and to provide a therapy thats best for that patient long term, he said.

Although younger patients with the disease tend to receive more intensive chemotherapy regimens, it is tougher to administer those same regimens to older patients because it can wipe out their blood cell counts and it is difficult to deliver in a safe way, Kadia explained. In addition, older patients are more likely to have comorbidities such as heart disease, diabetes or COPD, which must also be managed in an intensive chemotherapy setting.

In years past, the lower intensity therapies were more tolerable, but they were not associated with great response rates. However, with the recent Food and Drug Administration approval of Venclexta (venetoclax), overall response rates increased to 65% and complete remission rates now are in the range of 35% to 40% when combined with drugs such as decitabine or azacitidine), Kadia explained. He said that these regimens are associated with very, very good outcomes with a median survival of 14.5 months, and the older patients tolerate it better.

Typically, patients who have AML and are in remission undergo a stem cell transplant or bone barrow transplant. However, for an older patient, a transplant is too risky. Regardless, Kadia noted that their remission should be maintained. Maintenance therapy is then used in this population to keep their disease in remission. Maintenance therapy usually consists of low-intensity, long-term treatment that can maintain the diseases response and help prevent the leukemia from returning.

What most people need to realize is that most subsets of AML are incurable, he said. That means (the disease) will typically try to come back if not treated aggressively and long term. And so this maintenance therapy allows people to maintain remission once they have achieved it.

We have really had a revolution in the treatment of AML, where previously we only had two or three drugs to treat AML and many people got intensive chemotherapy, Kadia concluded. We are fortunate now to live in an era where we have nine new drugs approved just in the last five years.

For more news on cancer updates, research and education, dont forget tosubscribe to CUREs newsletters here.

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Orizuru Therapeutics Launches Operations as Research and Development-driven Company for Products Including induced Pluripotent Stem Cell (iPSC)…

Contributing to society and patients through the utilization of iPSC technology developed in Japan

New company to advance two successful outcomes from T-CiRA collaboration for severe heart failure and type I diabetes to clinical application of iPSC-based medicine

KYOTO, Japan, Aug. 10, 2021 /PRNewswire/ -- Orizuru Therapeutics Inc. ("OZTx") announced the launch of its operations on June 1, 2021. OZTx is a research and development-driven company focusing on the development of iPSCbased regenerative medicine and the application of iPSC technology, and is based at Shonan Health Innovation Park ("Shonan iPark").

In 2015, the Center for iPS Cell Research and Application ("CiRA") at Kyoto University and Takeda Pharmaceutical Company Limited ("Takeda Pharmaceutical") launched a joint research program, called T-CiRA, to accelerate research for the practical application of iPSC technology in drug development and regenerative medicine. The 10-year T-CiRA program has been led by Professor Shinya Yamanaka, Director of CiRA and Representative Director of the CiRA Foundation, with total funding of 20 billion yen in R&D from Takeda Pharmaceutical and human resources and facility-related support provided by Shonan iPark. Following the recent validation of pre-clinical efficacy of two cell therapy projects, CiRA and Takeda Pharmaceutical agreed to transfer the research assets from the projects to OZTx.

OZTx has two primary business areas of focus. First is the working toward the clinical application of the two cell therapy projects for which pre-clinical efficacy was validated in the T-CiRA program: the iPSC-derived cardiomyocyte project led by Project Leader Yoshinori Yoshida (Associate Professor at CiRA) and the iPSC-derived pancreatic islet cell project led by Project Leader Taro Toyoda (Junior Associate Professor at CiRA). In addition, OZTx has entered into a patent transfer and research asset license agreement with Kyoto University and Takeda Pharmaceutical, which own the intellectual property of iPSC-derived cardiomyocytes and iPSC-derived pancreatic islet cells, to research, develop, and provide regenerative medicine products for both projects.

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The second area of focus encourages the application of iPSC technology through the sharing of distinguished technologies in iPSC differentiation, culture, and purification, to rigorously support drug discovery research and develop the infrastructure for research in regenerative medicine. OZTx seeks to share its iPSC-related business activities broadly with communities and society, and also contribute to the delivery of iPSC-based regenerative medicine to patients and society in appropriate manners.

"We are very pleased that the innovative research outcomes from the T-CiRA collaboration where academic scientists and Takeda researchers work as one team are now transferred to OZTx toward their quick implementation," says Professor Yamanaka, Head of the T-CiRA program. To ensure continuity of research and development from T-CiRA, Professor Yamanaka has also been invited to chair the Scientific Advisory Board at OZTx. Dr. Yasushi Kajii, who oversees the T-CiRA collaboration on the Takeda side as Head of T-CiRA Discovery, also demonstrates his enthusiasm to collaborate with OZTx for implementation of the innovative iPSC technology, stating that, "I count on the establishment of OZTx so that pathways to bring outcomes from the T-CiRA collaboration to the bedside of patients suffering from intractable diseases can be strengthened."

OZTx is comprised of approximately 60 employees who have in-depth expertise in the latest iPSC technology as well as extensive experience in pharmaceutical R&D. Each of the 60 employees brings a strong commitment to the fore, demonstrating their passion and a sense of urgency to deliver iPSC technology to patients and society at large. The company is led by President, Representative Director, and Chief Executive Officer Kenji Nonaka, M.D., Ph.D. OZTx has raised a total of 6 billion yen through private placement with numerous partners listed below that stand in solidarity with OZTx's strong mission to put this Japan-born iPSC technology to practical use in regenerative medicine:

Seed round: Kyoto University Innovation Capital Co., Ltd. ("KYOTO-iCAP"), Takeda Pharmaceutical Company Limited, SMBC Venture Capital Co., Ltd.

Series A round: MUFG Bank, Ltd., SMBC Venture Capital Co., Ltd, MEDIPAL HOLDINGS CORPORATION, Sumitomo Mitsui Finance and Leasing Company Co. Ltd., Sumitomo Mitsui Trust Bank, Limited, Nippon Venture Capital Co., Ltd.

OZTx is committed to developing high quality products and services using the finest processes and seeks to contribute to society and patients by delivering regenerative medicine using iPSCs, which was first developed in Japan.

About iPSC-derived cardiomyocytes (iCM)

iCM was developed through a project led by Project Leader Yoshinori Yoshida, Associate Professor at CiRA. The cell is currently being refined for future clinical use, based on the cardiomyocyte differentiation method researched at CiRA and the myocardial purification method using small-molecule compounds developed in the T-CiRA program. iCM is a highly purified cardiomyocyte that demonstrated a high level of engraftment and safety in pre-clinical studies. When transplanted to the patient's heart, it is expected to supplement cardiomyocytes that are lost as diseases progress and accelerate the regeneration of cardiac muscles. iCM can potentially recover cardiac function in severe heart failure, which has been difficult to treat, as well as improve patients' quality of life and life prognosis.

About iPSC-derived pancreatic islet cells (iPIC)

The cell was developed after five years of research in the T-CiRA program, based on the method of inducing pancreatic cell differentiation discovered by Taro Toyoda, Junior Associate Professor at CiRA. iPIC are highly purified pancreatic endocrine cell aggregates that contain pancreatic beta cell-like cells, to the same extent as pancreatic islets in vivo. Once transplanted, it forms within the body pancreatic islet structures that include glucagon-positive cells and demonstrates physiological insulin secretion functions that respond to blood glucose levels. Thus, iPIC can potentially contribute to controlling the condition of patients with diabetes.

About Orizuru Therapeutics Inc. (OZTx)

OZTx, founded in April 2021 by KYOTO-iCAP, is steadfast in its dedication to bringing hope for better health through the infinite power of science. To deliver cell therapies to patients, the company promotes the wide use of cell therapy products and innovative iPSC-related technology through the following activities:

Development of regenerative medical products through cell transplantation

Support for drug discovery research and development of regenerative medicine research infrastructure using iPSC-related technology

For details, please refer to: https://www.orizuru-therapeutics.com/en/

About the Takeda-CiRA Joint Program for iPS Cell Applications (T-CiRA)

The agreement to form T-CiRA was reached in 2015 as a ten-year joint research program between CiRA and Takeda Pharmaceutical. Research activities commenced in 2016. With Takeda Pharmaceutical's funding of over 20 billion yen and the leadership of Professor Yamanaka, and researchers at CiRA, Tokyo Medical and Dental University, and RIKEN, multiple projects are being driven, including advanced research on the clinical application of iPSC technology for cancer, heart failure, diabetes, neuro-psychiatric disorders, and intractable muscle diseases. For details, please refer to: https://www.takeda.com/what-we-do/t-cira/

About the Center for iPS Cell Research and Application (CiRA), Kyoto University

CiRA was founded on April 1, 2010, at Kyoto University, as the world's first central research institute specializing in iPSCs. The institute is led by Professor Yamanaka, who serves as Director. With the aim of the medial application of iPSC, about 30 research groups engage in a range of research projects, including basic research, application research and bioethics research. For details, please refer to: https://www.cira.kyoto-u.ac.jp/e/index.html

About Kyoto University Innovation Capital Limited (KYOTO-iCAP)

KYOTO-iCAP, as a wholly-owned subsidiary of Kyoto University, provides investment and other business support to companies that utilize the results of research generated by Kyoto University and other national universities. KYOTO-iCAP currently manages the Innovation Kyoto 2016 Investment Limited Partnership ("KYOTO-iCAP No.1 Fund"), established in January 2016, with a total value of 16 billion yen, and the KYOTO-iCAP No.2 Fund, established in January 2021, with a total value of 18 billion yen. The KYOTO-iCAP No.1 Fund has a maturity of up to 20 years and the KYOTO-iCAP No.2 Fund has a maturity of up to 17 years, enabling the provision of long-term support for the practical application of the results of Kyoto University's strong fundamental research. In addition, the KYOTO-iCAP No.2 Fund will invest part of its funds in ventures originating from national universities other than Kyoto University. For more information, please visit https://www.kyoto-unicap.co.jp/en/

About Takeda Pharmaceutical Company Limited (Takeda Pharmaceutical)

Takeda Pharmaceutical is a global, R&D-driven pharmaceutical company that is committed to enhancing its R&D pipeline by strengthening its R&D activities, life cycle management, and partnerships and to fulfill its mission of contributing to better health for people and a brighter future for healthcare through high-quality pharmaceutical products.

For details, please refer to: https://www.takeda.com/

About Shonan Health Innovation Park (Shonan iPark)

Shonan iPark is a pharmaceutical company-driven science park founded by Takeda Pharmaceutical in April 2018. Housing organizations across the public and private sectors and academia that are diverse in business type and scale, the science park aims to accelerate innovation in healthcare. More than 120 companies and organizations including pharmaceutical companies as well as next-generation medicine, AI, venture capital, and government-related bodies, and more than 2,100 workers (as of August 2021) together form an ecosystem at Shonan iPark. For details, please refer to: https://www.shonan-health-innovation-park.com/en

SOURCE Orizuru Therapeutics Inc.

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Orizuru Therapeutics Launches Operations as Research and Development-driven Company for Products Including induced Pluripotent Stem Cell (iPSC)...

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Acute Myeloid Leukemia Treatment: What You Need to Know – Healthline

The umbrella term of leukemia encompasses several distinct types of leukemia, including acute myeloid leukemia (AML).

In 2021, its estimated that over 20,000 new cases of AML will be diagnosed, according to the National Cancer Institute (NCI). Since treatment varies depending on the specific kind of leukemia present, an accurate diagnosis is crucial.

There are a variety of treatments for AML. Your doctor will explain them and help choose a treatment plan based on the type of cancer you have and your individual situation.

Read on to learn more about the various treatment options for AML.

Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow. It affects white blood cells (WBCs), making them abnormal. In some forms of AML, they may also multiply very quickly.

Other names for AML include:

Read this for more information about AML.

Once the diagnosis is confirmed, your healthcare team will develop a plan to treat AML. Depending on the specific type and stage of AML, you may receive one or more of these treatments:

Chemotherapy is the main form of treatment for AML. Its divided into two phases:

Since AML can progress quickly, treatment is usually started as soon as possible after diagnosis. Other treatments may be used as well.

Chemotherapy, also called chemo, is the use of anti-cancer drugs to treat cancer. This is the main treatment for AML.

These drugs can be injected into a vein or under the skin, allowing the chemotherapy to travel through the bloodstream to attack cancer cells throughout the body. If leukemia has been found in the brain or spinal cord, chemo medication may be injected into the cerebrospinal fluid (CSF).

Chemo medications most often used to treat AML include:

Other chemo medications may include:

Side effects of chemotherapy can vary depending on the drug, dosage, and duration. They can include:

While chemotherapy is the main treatment for AML, for a subtype of AML called acute promyelocytic leukemia (APL), other non-chemotherapy drugs are more effective.

APL is caused by a specific gene mutation that affects WBCs. Some medications work better than chemo to help those cells develop normally. Two of these medications are:

ATRA can be given with chemotherapy or with ATO for the initial treatment of APL. Both drugs can also be given during consolidation.

Side effects of ATRA include:

Side effects of ATO can include:

Radiation therapy uses high-energy radiation to kill cancer cells. While its not the main treatment for those with AML, it can be used in treating AML. In AML, the radiation used is external beam radiation, which is similar to an X-ray.

Radiation can be used in AML to treat:

Side effects of radiation can include:

Surgery is rarely used in AML treatment. Leukemia cells are spread through the bone marrow and blood, making the condition impossible to improve with surgery. On rare occasions, a tumor or mass related to leukemia may form that may be treated with surgery.

Prior to chemotherapy, a small surgery to place a central venous catheter (CVC) or a central line, is often done. During this procedure, a small flexible tube is placed into a large vein in the chest. The end of it is either right under the skin or sticks out in the chest or upper arm.

Having a central line installed allows the treatment team to give intravenous medication and chemotherapy through the CVC, and to draw blood from it, reducing the number of needle sticks an individual has to have.

While chemotherapy is the main treatment for AML, it has its limits. Since high doses of these medications are toxic, the dosage must be limited. A stem cell transplant allows for higher doses of chemotherapy medications.

In a stem cell transplant, very high doses of chemotherapy medications, sometimes combined with radiation, are given. All of the individuals original bone marrow is destroyed on purpose.

Once this stage of therapy is over, blood-forming stem cells are given. These stem cells will grow, rebuilding the bone marrow. Healthy, cancer-free stem cells replace the destroyed bone marrow.

Read this article for more information about a stem cell transplant.

Targeted therapy drugs are medications that target only certain parts of cancer cells. They can be very effective for some people with AML. Most targeted therapy drugs are taken orally, except for gemtuzumab ozogamicin (Mylotarg), which is given as an intravenous infusion.

Talk with your treatment team about the potential side effects of each drug and what you should watch for when taking it. Some targeted therapy medications include:

One type of targeted therapy medication called FLT3 inhibitors targets the FLT3 gene. In some people with AML, a mutation in the FLT3 gene causes the creation of a protein, also called FLT3, that enables cancer cells to grow. Drugs in this category include:

Side effects of these drugs may include:

In some people with AML, there is a mutation in the IDH2 gene. These mutations stop bone marrow cells from maturing in a normal way. Medications called IDH inhibitors block IDH proteins produced by these mutated genes, allowing these bone marrow cells to grow normally and remain healthy.

Drugs in this category include:

Side effects can include:

AML cells contain a protein called CD33. A medication called gemtuzumab ozogamicin (Mylotarg) attaches to this CD33 protein and helps deliver chemotherapy medications directly to cancer cells so that these drugs are more effective.

Common side effects include:

There are less common but serious side effects like:

Venetoclax (Venclexta) is a BCL-2 inhibitor. This drug targets BCL-2, which is a protein that helps cancer cells live longer. The drug stops the BCL-2 protein from helping cancer cells survive so that these cancer cells die sooner. This medication can be used along with other chemotherapy drugs.

Side effects include:

AML can cause cellular mutations that prevent cells like bone marrow cells from developing and functioning normally. These mutations may affect the pathway cells use to send necessary signals. This pathway is called hedgehog. For some people with AML, especially those over age 75, strong chemo medications may be so harmful that chemo is not an option. For these individuals, a medication called, Glasdegib (Daurismo), may help them live longer. This medication helps stop the mutations and allows bone marrow cells to function normally.

Side effects of this medication may include:

Refractory AML happens when an individual is not in remission even after one to two cycles of induction chemotherapy, which means they have a blast count of 5 percent or more. Ten to 40 percent of people with AML have refractory AML.

If treatment isnt successful with one course of chemo, another one may be done. If a person is still not in remission after the second course of chemo, they may be given other medications or an increased dose of their current chemotherapy medications.

Other treatment options include stem cell transplant or a clinical trial of new therapies.

When an individual has no evidence of disease after treatment, its called remission or complete remission. Remission means these three criteria are met:

If there is no evidence at all of leukemia cells in the bone marrow, using highly sensitive tests, its called complete molecular remission. Minimal residual disease (MRD) occurs when, after treatment, leukemia cells cannot be seen in the bone marrow with standard tests but more sensitive tests like PCR tests do find leukemia cells.

Even after an individual has entered remission, they will likely need follow-up care and will need to be monitored by their doctor and healthcare team. This may mean additional tests, more frequent physical exams, and other care.

Although chemotherapy is the main treatment for AML, there are a variety of treatment options, depending on the AML subtype or whether you have a specific mutation. Treatment also depends on your response to initial treatment and whether or not remission is sustained.

Your treatment team will explain all of your treatment options and help you choose the treatment plan that is best for you and your individual situation.

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Acute Myeloid Leukemia Treatment: What You Need to Know - Healthline

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Vesole Discusses the Benefits and Challenges of Daratumumab in Patients With NDMM – Targeted Oncology

Vesole also looked at the challenges of adding daratumumab to a regimen for a patient eligible for transplant and the benefits of administering the treatment subcutaneously.

Benefits of Choosing Transplant in Patients With Newly Diagnosed Multiple Myeloma

David H. Vesole, MD, PhD: Im fortunate to be on a committee for the international transplant registry, and we published an article in Cancer looking at different age cut offs [during treatment].1 Was it safe? Was it effective? And did the patients have good long-term outcome? We looked at about 16,000 transplant [procedures] in North America over the past 10 years. [About] 2200 of them were patients over 70 years old, so we looked at over 70 vs less than 70 years old and the mortality rate was less than 1%. The response rate was identical. The progression-free survival [PFS] was identical for patients over and under 70 years old. Patients over 70 died, so the overall survival [OS] was shorter because they had other comorbidities and medical conditions over time.

We did another part of these data; the paper just got accepted in Cancer and looked at this group that was over 75 years old.2 It went from 2200 [patients who] were over 70 down to 450 who were over 75. [We saw the] same outcome. Now this is a very select group of patients that are handpicked, because only a smattering of those patients was over 75, but we looked at those 450 patients and the transplant-related mortality was still less than 1%. The response rates and the PFS were like those [younger] patients. So, age [by] itself is not a reason not to transplant.

Now, the latest [trend] is to give daratumumab with bortezomib [Velcade], lenalidomide [Revlimid], and dexamethasone [D-VRd]. I think most [physicians] would agree that triplets or quadruplets are the standard of care for a transplant-eligible patient. Were also going to talk about transplant-ineligible patients, and how to manage them. The number of treatment cycles varies in the ASCO [American Society of Clinical Oncology] guidelines. The comments from the experts, if you will, was 2 to 4 cycles. I will tell you, however, that I generally treat until they hit a plateau. With current regimens, you give D-VRd or KRd [carfilzomib (Kyprolis), lenalidomide, and dexamethasone], and most [patients] plateau by the third cycle. But I rarely give a 4-cycle therapy. Im not fixated on the number of cycles. I look at their response to the therapy, and then decide whether I should move them on to transplant.

Phase 3 CASSIOPEIA Trial (NCT02541383) Results

This used VTd [bortezomib, thalidomide (Thalomid), dexamethasone], transplant consolidation, and then theres a randomization, which is not important because I want to focus on the quadruplet therapy. [That quadruplet therapy is] daratumumab-VTd [D-VTd], transplant, followed by D-VTd, and then daratumumab maintenance.1

So, quadruplet vs triplet with the same basic schema. There were 1000 patients in this trial, and the quadruplet beats the triplet, even though [both groups would] get transplants. When they looked at minimal residual disease [MRD] negativity, using next-generation flow cytometry and next-generation sequencing [NGS]; in either instance, the 4-drug regimen had a superior MRD negativity compared [with] the 3-drug regimen, [64% vs 44% using flow cytometry and 57% vs 37%, respectively].

Outcomes of the GRIFFIN Trial

This is the same basic concept except were going to give them lenalidomide instead of thalidomide. [So, the treatment options are] D-VRd vs VRd. Patients get the induction for 1 to 4 cycles, they get a transplant, they get consolidation for 2 cycles, then they get randomized to daratumumab plus lenalidomide if they had daratumumab originally. Theres no crossover here. When you look at the D-VRd, the complete remission rate is 82% and when you look at the VRd alone, the combination is 61%. So it was a 20% improvement in the depth of response by giving D-VRd.3

Regarding sCR, the 4 drugs beat the 3 drugs, and when you look at the MRD negativity, the 4 drugs beat the 3 drugs, 62% vs 27%, respectively. Its a very potent regimen to give the quadruplet vs the triplet. When they did this, again, the follow-upwhich is not yet published, this is only presented as an abstract, so follow-up is not that long yetbut when they looked at the 24-month PFS rate, its not much different yet, and the OS is going to take years to show a difference.

When you give daratumumab on top of lenalidomide, I just want to point out that the neutropenia is higher when you give daratumumab, as it does cause neutropenia. Grade 3/4 neutropenia with the quadruplet, its 41% vs 22% with the triplet. The rest of the numbers are not that much different between the 2 groups, thrombocytopenia is a hair higher, but its mainly neutropenia that is significantly higher when you give daratumumab with lenalidomide.

Deciding the End Points When Looking at Salvage Therapy in Multiple Myeloma

I almost guarantee the OS will not be different between [other] studies, because we can salvage them with whatever they received. Back in the day, the FDA would only approve drugs based on OS, but because we now have so many salvage therapies, not just for myeloma, but breast cancer, lung cancer, etc., you cant really use OS because [were looking at] salvage therapies. You have to use the depth of response in this case, or the PFS, so most of the current myeloma trials use MRD negativity as their end point.

Our group believes in KRd, but even then, we dont give D-KRd because we cant get it approved. Even if we could, Im not sure that Id rather give it now, because Id rather use it as salvage therapy. The depth of response is better. If I did a D-KRd treatment vs KRd theres no doubt that you get a deeper response with the 4-drug regimen vs 3-drug regimen. Moreover, MRD negativity is a surrogate marker, but it really is a good predictor of remission duration, even if it doesnt predict OS.

Challenges With Adding Daratumumab and Continuing to Transplant

In the paper we submitted, in the over 75-year-old population doing transplant, the reviewer [pointed out that] if you look at daratumumab, lenalidomide, and dexamethasone [DRd] in the frontline setting, the response rate [was durable through 45 months]. [The reviewer commented,] if you can do that with DRd, why would we bother doing a transplant? I had to answer the reviewer, so I went back and looked at [these data and] the 2-year PFS rate with D-VRd, because thats when I had the data on, [it was a] 95% 2-year PFS rate.

With DRd without a transplant it was 80%, so is that a difference? A 15% difference in that larger population is significant, even though youre comparing across trials. But, to me, I think that really transplants shouldnt be going away because we have such effective salvage therapy.

The reviewer also mentioned that cost is an issue, [and recent comments showed that giving daratumumab upfront] is probably not cost effective, but as far as the duration of response, youre good because you can [use] salvage therapy for these patients.

These are unanswered questions of what the most cost-effective medicine really is. In the United States, its not a concern. Outside the United States, it is a major concern, and should everyone get treated with quadruplets? Because theres no doubt that the depth of response is better.

MAIA Study Efficacy and Safety Outcomes

On the DRd arm, were at 44 months compared with 41 months in VRd; at 4 years, the PFS rate is still 60%.5 So the PFS is going to be more than 48 months vs 41 months for VRd. [The DRd regimen has a longer PFS] and its got a better overall response rate, [compared with VRd] in the 80% range to 93%, so DRd has higher and more durable responses. Just keep that in mind when you have an older individual, and you dont get any peripheral neuropathy.

Even given once a week, or 3 weeks out of a month, you still get peripheral neuropathy even as the DRd regimen has deeper responses, longer responses than giving VRd when you try to compare across studies. While 60% of the patients were still in remission, the PFS has not been reached at 48 months, but it was far superior to the Rd. [These data are a given because] triplets essentially always beat doublets. This was true regardless of age, whether youre younger than 75 or over 75 years old, all these data favored the triplet vs the doublet.

When you give daratumumab with lenalidomide you get more neutropenia, grade 3/4 is 50% vs 35% for Rd alone (table6). The rest of the toxicities are comparable between the 2, but because you do get more neutropenia, you do get more infectious complications with the triplet vs the doublet.

Giving Daratumumab Subcutaneously vs Intravenously

The COLUMBA trial [NCT03277105] was what led to the subcutaneous formulation approval by the FDA.7 They took the original indication for daratumumab as a single agent for patients with relapsed/refractory disease. Relapsed/ refractory single agent [was given to patients with] 3 or more lines of prior therapy, half [received daratumumab] subcutaneously and half got it intravenously [IV].

They were looking for the response rate, as well as infusion reactions, which showed a difference between the 2 in a large trial of about 500 patients. What researchers found was that the response rates were identical between the subcutaneous and the IV delivery across the board. It was a noninferiority trial, and they proved it was noninferior, they were giving the daratumumab over 5 minutes. The toxicities were 25% to 30% infusion toxicities with the IV, and 10% to 12% in the subcutaneous arm.

There was another subcutaneous trial and if you look across the trials, the infusion reaction rate with IV daratumumab is about 30% diffusion, or the injection administration and reaction rate with subcutaneous is 11%. So, its safer, its faster, and the efficacy is identical. We converted 98% of our patients to subcutaneous treatment and all our newly started patients for months and months now are getting [treatment this way]. We still have a few older patients on IV, who just refuse because they say, Well, this ones working fine. Why would I want to change? They just refuse to change to the IV. Weve never had to switch someone back and forth.

REFERENCES

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Vesole Discusses the Benefits and Challenges of Daratumumab in Patients With NDMM - Targeted Oncology

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