RegulationPriority Review (United States), Breakthrough Therapy (United States), Orphan Drug (United States), Orphan Drug (European Union), Orphan Drug (Australia), Orphan Drug (United Kingdom)

Structure/Sequence

Sequence Code 315603822L

Source: *****

Sequence Code 315603823H

Source: *****

Clinical Trials associated with Crizanlizumab-TMCA

NCT06439082

/ RecruitingPhase 3

A Phase III, Multicenter, Randomized, Placebo Controlled, Double-blind Study to Assess Efficacy and Safety of Crizanlizumab (5 mg/kg) Versus Placebo, With or Without Hydroxyurea/Hydroxycarbamide Therapy, in Adolescent and Adult Sickle Cell Disease Patients With Frequent Vaso-Occlusive Crises

A phase III, multi-center, randomized, placebo-controlled, double-blind study to assess efficacy and safety of crizanlizumab (5 mg/kg) versus placebo, with or without hydroxyurea/hydroxycarbamide therapy, in adolescent and adult Sickle Cell Disease patients with frequent vaso-occlusive crises.

Start Date24 Oct 2024

Sponsor / Collaborator

Novartis Pharmaceuticals Canada, Inc.

NCT05469828

/ Not yet recruitingPhase 1/2IIT

Crizanlizumab Improves Tissue Oxygen Supply Demand Matching in Patients With Sickle Cell Anemia

Hypothesis
Efficient unloading of oxygen to regions of high metabolic demand requires a healthy microvasculature to sense local oxygen tension and regulate flow, accordingly. In sickle cell disease patients, the investigators have demonstrated oxygen supply-demand mismatch, or SDM, in proportion to anemia severity. SDM occurs in both the peripheral circulation and the brain, and four characteristics: 1) Hyperemia beyond expected for the level of anemia, 2) Corresponding loss of vascular dilatory reserve, 3) Impaired oxygen unloading to the tissues, and 4) Tissue hypoxia. In sickle cell disease, red blood cell (RBC) and white blood cell (WBC) adhere to vascular endothelium triggering transient or irreversible microvascular damage as well as releasing vasoactive substances that contribute to microvascular dysregulation. The investigators postulate that ongoing microvascular damage/dysregulation in the setting of increased total blood flow contributes to SDM. The investigators believe SEG101, by lowering RBC and WBC adhesion to the microvasculature, will improve SDM and tissue oxygenation.
Objectives
Primary - The investigators will test whether SEG101 improves SDM in patients with sickle cell anemia by measuring the change in tissue oxygenation measured by near infrared spectroscopy (NIRS).
Secondary/Exploratory - The investigators will identify end-organ disease and whether improvement of SDM by SEG101 occurs in patients with sickle cell anemia.

Start Date01 Jul 2024

Sponsor / Collaborator

Children's Hospital Los Angeles

[+1]

NCT05909618

/ RecruitingPhase 2IIT

An Open Label Phase 2 Study of Intravenously Administered Crizanlizumab Alone or in Combination With Nivolumab for Glioblastoma and Melanoma With Brain Metastases

A single-center, open-label, non-randomized phase I/II study to evaluate the efficacy, safety and tolerance of crizanlizumab monotherapy and in combination with nivolumab in patients with advanced glioblastoma (GB) who exhausted standard of care (SOC) therapy, patients with metastatic brain melanoma (MBM) and patients with newly diagnosed unmethylated GB.
Subjects will be screened for up to 28 days prior to treatment initiation. Eligible subjects will be allocated to one of 3 cohorts:
Cohort 1: Patients with metastatic melanoma with primarily diagnosed or newly progressing brain metastases who failed immunotherapy.
Cohort 2: Patients with recurrent or progressing GB following primary radiation therapy and temozolomide. Patients may have failed up to 2 prior systemic treatment lines (including temozolomide as adjuvant therapy) and are candidates for further treatment.
Cohort 3: Patients with newly diagnosed GB who were evaluated for methylguanine-DNA methyltransferase(MGMT) methylation status and have un-methylated MGMT promotor-therefore, they are not candidates for maintenance temozolomide therapy.

Start Date11 Jul 2023

Sponsor / Collaborator

Sheba Medical Center

100 Clinical Results associated with Crizanlizumab-TMCA

100 Translational Medicine associated with Crizanlizumab-TMCA

100 Patents (Medical) associated with Crizanlizumab-TMCA

118

Literatures (Medical) associated with Crizanlizumab-TMCA

10 Feb 2026·Blood Advances

Low bone mineral density and pain impact in adults with sickle cell disease

Article

Author: Wun, Ted ; Wu, Qian V. ; Adesina, Oyebimpe O. ; Zemel, Babette ; Nalbant, Hande ; Voutsinas, Jenna ; Nardo, Lorenzo ; Rokni, Mehrad ; Teos, Leyla Y.

Abstract:

Low bone mineral density (BMD) is a prevalent skeletal finding in sickle cell disease (SCD), but its clinical consequences are poorly understood. We hypothesized that low BMD, independent of osteonecrosis (ON), would associate with pain in adults with SCD. In the SCD Bone Pain study, 53 ambulatory adults (64% females; mean age, 38 ± 11 years; 66% hemoglobin [Hb] SS/Sβ0 thalassemia) underwent dual-energy X-ray absorptiometry scans of their lumbar spine, hip, forearm, and whole body. They also completed the Adult Sickle Cell Quality of Life Measurement Information System pain impact questionnaire. Twenty-three participants (43%) had low BMD, defined as lumbar spine, total hip, or femoral neck BMD z scores of −2 or less. In multivariate linear regression, lumbar spine BMD z scores significantly changed by +0.31, −0.29, −0.14, and −1.3 for every unit increase in Hb, indirect bilirubin, and white blood cell count, and with crizanlizumab use, respectively. Pain impact T-scores significantly decreased (worsened) by 6.0 and 6.5 with reduced estimated glomerular filtration rate and chronic opioid therapy but increased (improved) by 3.8 for every unit increase in serum phosphate. The median [interquartile range] pain impact T-scores were significantly lower in participants with low BMD and ON (38.3 [37.4, 40.1]) than those with either low BMD (49.5 [43.6, 54.4]; P = 3 × 10−5) or ON (52.7 [45.3, 57]; P = 2 × 10−4) alone. Whether sickle cell–related low BMD results from impaired bone formation and/or accelerated bone loss remains unclear. Understanding how low bone density, with or without ON, mediates SCD pain warrants further investigation. This trial was registered at www.clinicaltrials.gov as #NCT05283148.

01 Feb 2026·BRITISH JOURNAL OF HAEMATOLOGY

The enigma of sickle cell hepatopathy: Pathophysiology, clinical manifestations and therapy

Review

Author: Kaur, Navneet ; Batool, Saba ; Rizvi, Insia ; Wang, Jennifer ; Solipuram, Divya ; Komel, Aqsa

Summary:

Sickle cell disease (SCD) is one of the most common genetic disorders in the world predominantly affecting economically disadvantaged populations. There is a notable discrepancy between the growing adult SCD population and available diagnostic and therapeutic interventions for SCD. Sickle cell hepatopathy (SCH) is an all‐inclusive term to describe the acute and chronic liver manifestations of SCD. The pathophysiology of SCH follows no defined pattern or sequence that poses challenges to clinicians and researchers alike. Evidence is lacking for this underreported disease at various levels from diagnostic to therapeutic options. This paper reviews the basic pathophysiology, clinical features, biochemical and radiological findings of various SCH manifestations and outlines the management of each condition. Old and new therapy options in SCD including hydroxyurea, red blood cell exchange transfusion, ursodeoxycholic acid, voxelotor, l ‐glutamine and crizanlizumab have been reviewed to investigate the role of these options in treating SCH. The role of liver transplant, haematopoietic stem cell transplant and gene therapy in SCH patients have been reviewed.

21 Oct 2025·Cureus Journal of Medical Science

Emerging Therapies for Sickle Cell Disease: From Symptom Management to Curative Gene Therapy

Review

Author: Schiller, Gary ; Duesberg, Max S

Sickle cell disease (SCD) is a hereditary hemoglobinopathy caused by a point mutation in the β-globin gene, leading to the production of hemoglobin S and resulting in chronic hemolytic anemia, vaso-occlusion, and progressive organ damage. Affecting millions globally, with the highest prevalence in sub-Saharan Africa and other low-resource settings, SCD remains a major public health challenge. Current therapies, including hydroxyurea, L-glutamine, crizanlizumab, and transfusions, primarily offer symptomatic relief but do not correct the underlying genetic defect. Hematopoietic stem cell transplantation remains the only established cure but is limited by donor availability and associated risks. Recent advances in gene therapy have transformed the therapeutic landscape of SCD, offering curative potential through techniques such as lentiviral vector-mediated gene addition and CRISPR/Cas9 gene editing. These approaches aim to restore normal hemoglobin production or reactivate fetal hemoglobin expression. While clinical trial outcomes are encouraging, with reduced vaso-occlusive crises and transfusion independence, major challenges remain, including high costs, need for myeloablative conditioning, and limited access in high-burden regions. This review explores the evolution of SCD treatment, evaluates the promise and limitations of emerging gene therapies, and highlights the urgent need for equitable access to these transformative technologies.

News (Medical) associated with Crizanlizumab-TMCA

06 Mar 2025

·endpts.com

Novo Nordisk’s rare disease ‘company within a company’ has an open goal in sickle cell

Novo Nordisk is known for making therapies for some of the world’s most prevalent conditions, but it’s also working on candidates for some of the least common. Though the company’s rare disease unit is active in hemophilia and endocrine disorders, one of its most interesting up-and-coming assets is intended for sickle cell disease. Ludovic Helfgott, Novo’s head of rare disease, told Endpoints News on Thursday that data from a late-stage trial of etavopivat in sickle cell should come next year. That readout will indicate if the drug can overcome the worrying precedents set by other sickle cell treatments and whether Novo’s $1.1 billion buyout of Forma , which developed etavopivat, was in fact a good move. The company is targeting a 50% cut in the rate of vaso-occlusive crises (VOCs) in etavopivat’s Phase 3 study, according to Helfgott. This is roughly in line with the 46% cut in VOCs that the pyruvate kinase activator demonstrated in Phase 2 . In a Dec. 10 note, Leerink analysts said etavopivat’s VOC reduction in the mid-stage trial narrowly met the bar for clinical meaningfulness. However, they also wrote that etavopivat may have an important place in the sickle cell market given the high unmet need after Pfizer pulled its sickle cell drug Oxbryta worldwide last year over safety concerns. Plus, Europe and the UK a year ago rescinded approval of Novartis’ sickle cell therapy Adakveo, citing a no longer favorable “benefit-risk balance.” Helfgott is clear that Oxbryta’s withdrawal has no read-through to etavopivat. “We have a complete different molecule,” he said. “From a safety perspective, what Pfizer decided to do has no implication on what we do. It’s a completely different mode of action.” From a public health perspective, however, he noted that “it’s never a good thing when a medicine is withdrawn.” Patients have fewer treatment options, and Helfgott also said that there has been “a bit of mistrust in medicines” among sickle cell patients in recent years “and having a medicine withdrawn, unfortunately, doesn’t really help that.” Even with the much-anticipated arrival of sickle cell gene therapies, uptake has been slow. Vertex Pharmaceuticals’ Casgevy is slowly taking off , though it’s not a viable therapy for most sickle cell patients, who live in developing countries and have no way of paying roughly $2 million for treatment. Then there’s bluebird bio’s Lyfgenia, which stalled commercially. The biotech was sold to investors last month for just $29 million upfront. If etavopivat’s Phase 3 data are good enough for approval, it could have a pretty clear run at the sickle cell market, particularly if it shows a benefit on a secondary endpoint. The trial aims to demonstrate that the therapy can reduce the organ damage from sickle cells’ inability to deliver oxygen to patient tissues. “If you can show that you can preserve the organs better, then you have something which, for me, is really clinically relevant,” Helfgott said. Novo is investing heavily in its rare disease unit, which Helfgott refers to as “a company within a company.” It brings in around 8% to 10% of Novo’s annual revenue but accounts for more than 14% of the pharma’s R&D spend. The products it is developing are at least partly a hedge against hard times ahead. “The bigger the obesity [market], the bigger the diabetes [market], the bigger you need to compensate when loss of exclusivity will happen,” Helfgott said. “It’s really a strategic play for Novo Nordisk to have the rare disease segment alongside the more prevalent diseases.”

Phase 3Gene TherapyClinical ResultCell TherapyPhase 2

21 Oct 2024

·www.biospace.com

5 Sickle Cell Therapies to Watch Following Pfizer’s Oxbryta Exit

iStock/ YuLi4ka In the wake of Pfizer’s voluntary market withdrawal of the popular sickle cell disease therapy, BioSpace looks at five investigational drugs currently making their way through the pipeline. A recent fumble has left the sickle cell disease community reeling . Last month, Pfizer abruptly pulled Oxbryta from all global markets after new data showed a higher risk of deaths and complications in treated patients. “[Oxbryta] was one of four medications which we would describe as disease-modifying,” Clifford Takemoto, director of clinical hematology at St. Jude Children’s Research Hospital, told BioSpace . Since the approval of Bristol Myers Squibb’s hydroxyurea for sickle cell disease (SCD) in 1998, only three disease-modifying medications have entered the market, he said. Oxbryta, which won FDA accelerated approval in November 2019, was one of these. Another, Novartis’ Adakveo, has also been called into question after failing to reduce vaso-occlusive crises (VOC) in people with SCD in a Phase III trial last year. EU regulators formally revoked Adakveo’s approval in August 2023, but it remains available in the U.S. “We were optimistic that things were changing,” Takemoto said. “People had hoped that these medications would make a difference.” SCD affects more than 100,000 people in the U.S. and 8 million worldwide. With so few treatment options, it remains a seriously underserved population . Takemoto said the Oxbryta withdrawal has left some patients a “bit angry” and distrustful of new medications, and the question for the community remains: “What’s next?” For Takemoto, the ultimate hope for SCD treatment lies in next-gen transplantation and gene therapy. With the approval of bluebird bio’s Lyfgenia and Vertex and CRISPR Therapeutics’ Casgevy, the potential for gene therapies in SCD is there, even if the rollout is slow and for most, not very accessible, he said. St. Jude is developing its own gene therapy, which the research hospital hopes to move into clinical trials sometime next year. Takemoto also pointed to work being done in bone marrow transplantation intended to reduce toxicity and improve success rates. St. Jude is working on a process that will utilize a “half match,” where a parent’s bone marrow can be used instead of a sibling. These treatments could be transformative, Takemoto said. Here, BioSpace looks at five investigational therapies making their way through the SCD pipeline. Pfizer’s Inclacumab and Osivelotor Oxbryta is not the only SCD asset Pfizer brought onboard with its 2022 acquisition of Global Blood Therapeutics . Two other investigational therapies, inclacumab and osivelotor, were also part of the deal. Inclacumab, a P-selectin inhibitor, is currently being assessed in a Phase III trial to determine its safety and efficacy in reducing VOC. The drug works by binding to P-selectin, a cell adhesion molecule found on platelets. According to Pfizer, this prevents platelets from aggregating, which in turn, is expected to help maintain normal blood flow. Like Oxbryta, osivelotor is a sickle hemoglobin polymerization inhibitor, but with a next-generation design. The asset is currently being studied in a Phase II/III study slated for completion in 2028. While Pfizer has not stated whether the recent findings related to Oxbryta will impact the development of osivelotor, Leerink Partners noted that a Phase II study raised safety concerns, with treatment-emergent adverse events seen in 8 out of 35 patients. Agios Pharmaceuticals’ Mitapivat Agios Pharmaceuticals is developing mitapivat, a pyruvate kinase (PK) activator that is already approved for the treatment of hemolytic anemia in adults with PK deficiency, for SCD. Red blood cells require the PK enzyme for energy, Takemoto explained. In December 2023, the company presented positive data from the Phase II portion of its pivotal RISE UP study. The annualized rate of sickle cell pain crises for patients in the higher dose treatment arm was 0.51 compared to 1.71 for participants in the placebo arm. Takemoto said the oral medication seems to benefit red blood cell health in general and noted that the data look favorable for patients with SCD and other hemolytic anemias. But not everyone is as convinced. Leerink Partners analysts wrote last month of concerns that similar physiological effects could be seen with both Oxbryta and mitapivat. A Phase III readout is expected next year, and the company is targeting a label expansion in 2026. Novo Nordisk’s Etavopivat In 2022, Novo Nordisk paid $1.1 billion to acquire Forma Therapeutics, gaining a lead SCD asset, etavopivat, in the deal. Like mitapivat, etavopivat is also a PK activator, but Novo’s candidate comes with a potential advantage —once daily dosing, versus mitapivat’s twice daily regimen. Etavopivat is currently being studied in a Phase III trial slated for completion in 2026. Phase I data presented by Forma at the American Society of Hematology’s annual meeting in 2021 showed a “sustained increase in hemoglobin and improvement in biomarkers of hemolysis and red blood cell health.” The results, from 15 patients dosed for up to 12 weeks, also showed a trend toward decreasing VOC compared to the 12 months prior to their entering the trial. Takemoto said the candidate “looks very promising” so far but acknowledged that “there are things we don’t know about it. We may learn new side effects as it’s used.” St. Jude will serve as a site for the Phase III trial. Fulcrum Therapeutics’ Pociredir Fulcrum Therapeutics ’ pociredir, a polycomb repressive complex 2 (PRC2) inhibitor, is designed to induce expression of fetal hemoglobin to compensate for the mutated hemoglobin that occurs in SCD. The development path for pociredir has not been without bumps. In February 2023, the FDA slapped Fulcrum with a clinical hold based on previously submitted preclinical data and non-clinical and clinical evidence of hematological malignancies observed with other PRC2 inhibitors. The hold was released six months later. The small molecule, which is currently being studied in a Phase Ib trial, has been well-tolerated in people with SCD with no treatment-related adverse events reported after up to three months exposure, according to a press release announcing the lifted clinical hold.

Clinical ResultPhase 3Phase 2Drug ApprovalPhase 1

26 Sep 2024

·www.outsourcing-pharma.com

Pfizer withdraws sickle cell disease drug Oxbryta amid safety concerns

The withdrawal decision was prompted by clinical data indicating that the overall benefit of Oxbryta “no longer outweighs the risk” in its target patient population, the company said in a public release . Specifically, the trials outline an “imbalance” in vaso-occlusive crises and fatal events that the company will assess further. The move to stop clinical trials of the drug will last while Pfizer further reviews the available data and investigates the findings. Sickle cell disease is a genetic blood disorder where patients have a mutation in hemoglobin, a protein found in red blood cells. This leads the protein to clump together, causing cells to have a sickle shape that can block blood vessels and carry less oxygen, leading to acute pain and anemia. Oxbryta, whose generic name is voxelotor, is an oral small molecule drug that was first approved by the US Food and Drug Administration (FDA) for the treatment of sickle cell disease in 2019, with an EU approval granted in 2022. The drug is designed to make hemoglobin better at carrying oxygen and less prone to clumping together, making red blood cells more functional. The treatment was previously developed by the U.S. firm Global Blood Therapeutics before the company was snapped up by Pfizer for $5.4 billion in 2022 , and bagged Pfizer $328 million in revenues in 2023 . The big pharma company has notified regulators about the data and doesn’t expect the event to impact its full-year 2024 financial guidance. Nevertheless, the company’s stock price on the New York Stock Exchange slumped by more than 1% at the news yesterday (Wednesday 25th September). googletag.cmd.push(function () { googletag.display('text-ad1'); }); Emphasizing Pfizer’s focus on patient safety, chief medical officer and head of worldwide medical and safety, Aida Habtezion, said in the company release that the Pfizer’s “primary concern is for patients who suffer from SCD, which remains a very serious and difficult-to-treat disease with limited treatment options. We advise patients to contact their physicians to discuss alternative treatment while we continue to investigate the findings from our review of the data.” The global market for sickle cell disease was worth $2.25 billion in 2022 and is expected to grow by 20.1% per year to $9.84 billion by 2030. The main players in the market have included Pfizer with Oxbryta, Novartis with the antibody Adakveo (crizanlizumab) and Generex Biotechnology’s Emmaus Medical with Endari (L-glutamine). In 2017, Endari became the first branded drug for sickle cell disease in decades when it was greenlit by the U.S. FDA. Another driver for the sickle cell disease market is gene therapy, with the first cell-based gene therapies – Casgevy by Vertex Pharmaceuticals and Lyfgenia by Bluebird Bio – approved by the U.S. FDA in late 2023 .

Drug ApprovalGene Therapy

100 Deals associated with Crizanlizumab-TMCA

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KEGG	Wiki	ATC	Drug Bank
-	Crizanlizumab-TMCA	B06AX01	DB15271

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Anemia, Sickle Cell	United States	Novartis Pharmaceuticals Corp.	15 Nov 2019
Vaso-occlusive crisis	United States	Novartis Pharmaceuticals Corp.	15 Nov 2019

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Sickle Cell Trait	Phase 3	Netherlands	Novartis Pharma AG	03 May 2021
COVID-19	Phase 2	United States	Novartis AG	09 Jul 2020
Priapism	Phase 2	United States	Novartis Pharmaceuticals Corp.	16 Oct 2019
Myelofibrosis	Phase 2	Australia	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Canada	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Denmark	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Germany	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Hungary	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Italy	Novartis Pharmaceuticals Corp.	26 Sep 2019
Myelofibrosis	Phase 2	Netherlands	Novartis Pharmaceuticals Corp.	26 Sep 2019

Clinical Result

Indication

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT06439082 (SPARKLE, ASH2025)	Phase 3	Anemia, Sickle Cell	315	Crizanlizumab 5.0 mg/kg	qdyuzcquit(idaukckifi) = bcwjkhqeit qjkmpafkrz (oykzvambmj ) View more	Positive	06 Dec 2025
				Placebo	qdyuzcquit(idaukckifi) = jpihqrmwmb qjkmpafkrz (oykzvambmj ) View more
PS2172 (EHA2025)	Not Applicable	P-selectin	994	Crizanlizumab (Complete biologic responders)	lfhpzllvov(jjfyihryhs) = wcocukqumj xptvqhbtha (edjwtwgpgm )	Positive	14 May 2025
				Crizanlizumab (Incomplete biologic responders)	lfhpzllvov(jjfyihryhs) = ocmhpibxjc xptvqhbtha (edjwtwgpgm )
NCT03814746 (STAND, Pubmed) Manual	Phase 3	Anemia, Sickle Cell	252	crizanlizumabcrizanlizumab 5.0 mg/kg	nvtfnzwshv(cvbllspsxi) = ljvwozzkum cvbrjvbkmi (xmkorqwcip, 1.90 - 3.26) View more	Negative	01 Apr 2025
				crizanlizumabcrizanlizumab 7.5 mg/kg	nvtfnzwshv(cvbllspsxi) = xrrwubigbb cvbrjvbkmi (xmkorqwcip, 1.56 - 2.65) View more
NCT03938454 (SPARTAN, CTgov)	Phase 2	Priapism \| Anemia, Sickle Cell	36	Crizanlizumab	yrjnxqgcpt(qnnrlkrkbt) = lifubkgiug ylypxgyeaz (zfnasflcag, xobsqcoxct - avcrnmgunt) View more	-	10 Mar 2025
NCT04662931 (CTgov)	Phase 4	Vaso-occlusive crisis \| Anemia, Sickle Cell	140	Crizanlizumab	pinfmikmgq = kfxpcxersm sybjmbtahk (bflxitabwo, zmlxdmzpby - prcoiqooql) View more	-	08 Jan 2025
ASH2024	Not Applicable	Anemia, Sickle Cell	-	Crizanlizumab 5.0 mg/kg	dqxqvemtlm(epxrcyyqlv) = dkwmdbeeda pwrrvvtmny (rgntahuctk ) View more	-	07 Dec 2024
				Crizanlizumab 8.5 mg/kg	dqxqvemtlm(epxrcyyqlv) = taeidxlgpp pwrrvvtmny (rgntahuctk ) View more
ARVO2024	Phase 2	Vasculopathy, Retinal, With Cerebral Leukodystrophy	10	Crizanlizumab 5 mg/kg	fbqojpbbnd(ojtparapwd) = No patients experienced severe adverse events, with mild to moderate events attributed to constitutional symptoms (48%) or gastrointestinal symptoms (35%). xuidjeqtey (gikhrthkwz )	Positive	05 May 2024
NCT03264989 (SOLACE-adults, CTgov)	Phase 2	Anemia, Sickle Cell	57	Crizanlizumab (Crizanlizumab 5.0 mg/kg)	gvyqklnidr(jgkhcixhih) = nfooipfecf bamsmzcaof (umquokyhnd, 2810) View more	-	23 Apr 2024
				Crizanlizumab (Crizanlizumab 7.5 mg/kg)	tzhebxxqod(ouothakdpu) = livcdjabbl mkwalfpghz (aspskhtevg, ttbxeadtkz - yhzoyunvce) View more
NCT03814746 (STAND, CTgov)	Phase 3	Anemia, Sickle Cell	255	Crizanlizumab (SEG101) (Crizanlizumab (SEG101) at 5.0 mg/kg)	qwmpylerzy(ncwooprdwt) = qykxckhegy lfxlnvhzad (pfqqsctaeo, 2.98) View more	-	08 Jan 2024
				Crizanlizumab (Crizanlizumab (SEG101) at 7.5 mg/kg)	qwmpylerzy(ncwooprdwt) = dtysipnuhb lfxlnvhzad (pfqqsctaeo, 2.30) View more
NCT03264989 (SOLACE-adults, Pubmed \| Ther Adv Hematol)	Phase 2	Anemia, Sickle Cell	57	Crizanlizumab 5.0 mg/kg	huzvpveydm(frhzdvzdsz) = aqcplrfgyh slpjerfhob (atbiixlzxk )	Positive	01 Jan 2024
				Crizanlizumab 7.5 mg/kg	huzvpveydm(frhzdvzdsz) = olznjdmcsb slpjerfhob (atbiixlzxk )

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