A Randomized Phase 3 Study to Compare VAC (Higher Cyclophosphamide Dose and Intensity) Versus VAC/VI (Lower Cyclophosphamide Dose and Intensity) Plus Maintenance Therapy in Patients With Newly Diagnosed Intermediate-Risk Rhabdomyosarcoma

This phase III trial compares higher dose chemotherapy, with vincristine, dactinomycin and cyclophosphamide, over a shorter amount of time to lower dose chemotherapy plus maintenance, with vincristine, dactinomycin, cyclophosphamide, irinotecan and vinorelbine, over a longer amount of time, along with standard of care surgery and radiation, in patients with newly diagnosed intermediate risk rhabdomyosarcoma. Vincristine and vinorelbine are in a class of medications called vinca alkaloids. They work by stopping tumor cells from growing and dividing and may kill them. Dactinomycin is a type of antibiotic that is only used in cancer chemotherapy (antineoplastic antibiotic). It works by damaging the cell's DNA and may kill tumor cells. Cyclophosphamide is in a class of medications called alkylating agents. It works by damaging the cell's DNA and may kill tumor cells. It may also lower the body's immune response. Irinotecan is in a class of antineoplastic medications called topoisomerase I inhibitors. It blocks a certain enzyme needed for cell division and DNA repair and may kill tumor cells. It is not yet known if the higher dose chemotherapy over a shorter amount of time or the lower dose chemotherapy with maintenance over a longer amount of time is more effective in the treatment of patient with newly diagnosed, intermediate risk rhabdomyosarcoma.

Start Date14 Jul 2026

Sponsor / Collaborator

The Children's Oncology Group Foundation, Inc.

CTIS2025-524728-22-01

/ Not yet recruitingPhase 1/2IIT

ACTIVATE - Phase 1 Clinical Trial evaluating the combination of Actinomycin D and venetoclax in patients with Relapsed/Refractory (R/R) Acute Myeloid Leukemia (AML)

Start Date01 Jun 2026

Sponsor / Collaborator

Assistance Publique Hopitaux De Paris

NCT07194044

/ RecruitingPhase 1IIT

Metastatic Ewing's Trial Testing Schedule Enhancement to Improve Outcomes

This single arm study is designed to demonstrate the feasibility of a radically different approach for an exceptionally high-risk subset of MES with widely metastatic disease (WMES). We incorporate the use of evolutionary principles that apply to species and population dynamics as related to adaptation and extinction to populations of cancer cells that similarly adapt and that we are attempting to make extinct, resulting in a cure for the patient. Such principles include an initial intense first strike to deplete the bulk of the cancer cells, followed by a series of sequential second strikes towards eliminating residual, resistant populations, followed by a prolonged period of maintenance chemotherapy to eliminate any remnant cells, using agents generally regarded to be active against newly diagnosed ES.

Start Date05 Feb 2026

Sponsor / Collaborator

H. Lee Moffitt Cancer Center & Research Institute, Inc.

100 Clinical Results associated with Dactinomycin

100 Translational Medicine associated with Dactinomycin

100 Patents (Medical) associated with Dactinomycin

17,801

Literatures (Medical) associated with Dactinomycin

01 Dec 2026·CELLULAR SIGNALLING

METTL14-mediated m6A modification of CCNE1 accelerates progression of myelodysplastic syndromes via MAPK-ERK and PI3K-AKT signaling pathways

Article

Author: Liang, Xiaolin ; Yao, Yibin ; Xiang, Xiaoyun ; Luo, Jun ; Yang, Xiaobo ; Liu, Zhenfang ; Wu, Man ; Tang, Zhongyuan ; Luo, Jiamin ; Huang, Yiqian ; Huang, Xiaoke ; Cheng, Peng ; Li, Chunrui ; Zhu, Shanhu ; Lu, Na ; Zhang, Qiquan

BACKGROUND:

N⁶-methyladenosine (m⁶A) is the most common RNA modification and plays a key role in the initiation, progression, and relapse of multiple cancers, including hematologic malignancies. However, the role of m⁶A and m⁶A regulatory genes in myelodysplastic syndromes (MDS) remains unclear. This study aims to elucidate the function and molecular mechanism of methyltransferase METTL14 in MDS.

METHODS:

RT-qPCR was used to assess the expression of multiple m⁶A regulators, focusing on METTL14 in MDS patients and cell lines. METTL14 overexpressing and knockdown cell lines were established, and CCK-8, EdU, and flow cytometry assays were performed to explore the biological functions of METTL14.Dot blot, MeRIP-Seq, MeRIP-qPCR, RT-qPCR, and Western blot were employed to investigate the underlying molecular mechanism.

RESULTS:

Dysregulation of multiple m⁶A regulators was observed in MDS, among which METTL14 was upregulated. Elevated METTL14 expression increases MDS risk and adverse prognosis, emerging as a biomarker for poor prognosis. METTL14 promoted proliferation and cell-cycle progression of MDS cells while inhibiting apoptosis; corresponding changes were observed in cell cycle and apoptosis markers. METTL14 regulated cellular m⁶A levels. Downstream targets of METTL14 were enriched in cell cycle-related pathways, with CCNE1 identified as a critical target. Knockdown of METTL14, actinomycin D, or S-adenosylhomocysteine treatment reduced CCNE1 mRNA and protein levels. Furthermore, METTL14 activated MAPK-ERK and PI3K-AKT signaling via CCNE1 in an m⁶A-dependent manner, thereby promoting proliferative MDS cells' capacity.

CONCLUSIONS:

This study delineates a METTL14/m⁶A/CCNE1 signaling axis in MDS progression and suggests that METTL14-mediated m⁶A modification may be a potential therapeutic target for MDS.

01 Dec 2026·JOURNAL OF BIOENERGETICS AND BIOMEMBRANES

FTO-mediated GPX4 m6A modification in ferroptosis-induced DNA damage and inflammatory response during acute lung injury

Article

Author: Liu, Xiuli ; Yuan, Fang ; Gu, Ying

To investigate the role of Fat Mass and Obesity-associated Protein (FTO) in acute lung injury (ALI) and elucidate how it regulates ferroptosis via N6-methyladenosine (m6A) modification of glutathione peroxidase 4 (GPX4). ALI models were established in LPS‑stimulated BEAS‑2B cells and mice. FTO expression was modulated by siRNA, inhibitors, or adeno‑associated virus. Ferroptosis, apoptosis, inflammation and DNA damage were assessed by RIP‑qPCR, meRIP‑qPCR, Western blotting and TEM. GPX4 m6A site mutants were constructed. GPX4 mRNA/protein stability and translation were analyzed using actinomycin D and cycloheximide. Establish an LPS-induced ALI mouse model, perform adeno-associated viral knockdown of FTO in lung tissue, and validate in vivo using GPX4 inhibitors. FTO inhibition significantly attenuated LPS-induced ferroptosis, apoptosis, inflammatory responses, and mitochondrial damage. Mechanistically, FTO accelerates GPX4 protein degradation by reducing m6A modification of GPX4, thereby downregulating GPX4 protein expression in a post-transcriptional and post-translational manner. This leads to intracellular iron accumulation, ROS bursts, lipid peroxidation, and DNA damage. Mutating the m6A site in GPX4 or supplementing GPX4 protein effectively reverses the aforementioned damage. Silencing FTO in vivo significantly ameliorates pulmonary tissue pathology, impaired lung function, ferroptosis, and inflammatory responses in mice via a GPX4-dependent pathway, whereas GPX4 inhibition reverses this protective effect. FTO exacerbates ALI by mediating m6A modification of GPX4 and downregulates its protein expression, thereby driving ferroptosis and DNA damage. Targeting the FTO-GPX4 axis may offer novel therapeutic strategies for ALI.

01 Dec 2026·Biochimica et Biophysica Acta-Gene Regulatory Mechanisms

BTRC aggravates FFA-induced lipid accumulation in MASLD via G3BP1 degradation and subsequent SIRT6 mRNA destabilization

Article

Author: Meng, Lingyu ; Zou, Dongmei ; Wu, Yuandong ; Liu, Liang ; Yang, Chengyang

BACKGROUND:

Metabolic dysfunction associated steatotic liver disease (MASLD) features hepatic steatosis and lipotoxicity, yet its molecular mechanisms remain incompletely understood. How post-transcriptional regulation and protein turnover shape hepatocyte lipid homeostasis in MASLD requires further elucidation.

METHODS:

For in vivo and in vitro validation, C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks, while HepG2 cells were exposed to free fatty acids (FFA) to induce steatosis. Lipid accumulation and viability were assessed by Oil Red O/BODIPY staining, triglyceride assays, and CCK-8. Mechanisms were explored using RIP and RNA pulldown to verify G3BP1 binding to SIRT6 mRNA, and actinomycin D to determine mRNA stability. BTRC-mediated ubiquitination and degradation of G3BP1 were validated by Co-IP, CHX, and MG132 assays. The lipid metabolism proteins were assessed by Western blotting.

RESULTS:

FFA downregulated G3BP1 and SIRT6 and increased BTRC. G3BP1 overexpression preserved viability, reduced lipid droplets and triglycerides, restored CPT1A and PPARα, and suppressed SREBP-1c and FAS. G3BP1 bound SIRT6 mRNA and stabilized SIRT6. BTRC interacted with G3BP1 and promoted its ubiquitination; Functionally, BTRC silencing alleviated FFA-induced lipid accumulation and metabolic dysregulation while elevating G3BP1 and SIRT6; concomitant SIRT6 knockdown abrogated these benefits. In HFD-fed mice, AAV-mediated BTRC silencing alleviated HFD-induced hepatic steatosis and liver injury.

CONCLUSION:

A BTRC-G3BP1-SIRT6 axis governs hepatocyte lipid homeostasis under lipotoxic stress. BTRC promotes steatosis by degrading G3BP1, thereby destabilizing SIRT6 mRNA and impairing fatty acid oxidation. Targeting BTRC or reinforcing G3BP1/SIRT6 offers a potential therapeutic strategy for MASLD.

News (Medical) associated with Dactinomycin

10 Apr 2026

·www.mironova.com

Non-Prostaglandin Hair Growth Science in 2026: What We Know, What We Still Need

The non-prostaglandin hair active category has grown rapidly over the past several years, driven partly by genuine scientific interest in alternative follicular mechanisms and partly by regulatory pressure on prostaglandin analogs in cosmetic applications. The EU Scientific Committee on Consumer Safety has concluded that several prostaglandin analogs — including MDN, isopropyl cloprostenate, and DDDE — cannot be considered safe for cosmetic use in lash and brow growth products. Health Canada already prohibits prostaglandins in cosmetics outright. In the United States, the FDA has issued warning letters and secured a $2.3 million settlement against companies marketing prostaglandin-containing products with drug-like claims. Against this regulatory backdrop, ingredients from the 2,4-diaminopyrimidine N-oxide class have attracted renewed attention. Three molecules in particular — PDPO (pyrrolidinyl diaminopyrimidine oxide), DPO (diaminopyrimidine oxide, commonly known as aminexil), and OTZ (L-2-oxothiazolidine-4-carboxylic acid, known as procysteine) — form the basis of a multi-target formulation strategy. But attention is not evidence, and the temptation to flatten complex pharmacology into simple marketing claims has created real problems in this space. This article separates what is established in the peer-reviewed literature from what remains inferential, and examines what that distinction means for product development teams working in this category. PDPO (CAS 55921-65-8, MW 195.22) differs from minoxidil (CAS 38304-91-5, MW 209.25) by a single structural modification: a pyrrolidine ring at the C6 position where minoxidil carries a piperidine ring. Both compounds share the identical 2,4-diaminopyrimidine-3-oxide pharmacophore — the structural motif associated with potassium channel opening activity. The biology of that pharmacophore is well established. Shorter et al. (2008, FASEB Journal) mapped ATP-sensitive potassium channel subunits across human hair follicle compartments, identifying Kir6.1/SUR2B channels in dermal papilla cells and connective tissue sheath, and Kir6.2/SUR1 channels in epithelial matrix keratinocytes. Minoxidil sulfate is selective for SUR2-containing channels, acting primarily on dermal papilla. The genetic validation is striking: Cantú syndrome, caused by gain-of-function mutations in ABCC9 (encoding SUR2), produces congenital hypertrichosis — direct proof that constitutive SUR2 activation promotes hair growth in humans. Downstream, minoxidil's follicular effects are multi-modal. Lachgar et al. (1998, British Journal of Dermatology) demonstrated dose-dependent VEGF mRNA upregulation — up to approximately six-fold at 24 µM in dermal papilla cells. Kwack et al. (2011, Journal of Dermatological Science) showed that minoxidil activates β-catenin signaling in human dermal papilla cells via GSK3β phosphorylation. Marubayashi et al. (2001, Journal of Investigative Dermatology) identified SUR2B expression in dermal papilla cells and proposed adenosine-mediated signaling as an intermediary mechanism. At the proliferative level, minoxidil at 0.1–1.0 µM increases dermal papilla cell proliferation by 60–108% and activates ERK phosphorylation by 287–351%. The problem is that none of this has been demonstrated for PDPO specifically. No published peer-reviewed study reports PDPO's EC₅₀ for K_ATP channel opening, its SUR subtype selectivity, whether it requires sulfotransferase activation (as minoxidil does via SULT1A1), or its effects on any isolated cell type or follicular tissue. The sole clinical evidence comes from multi-ingredient formulations — primarily the Spectral DNC-N study (Draelos et al., 2019, Skin Appendage Disorders), an open-label trial of 49 women using a product containing PDPO alongside azelaic acid, lysophosphatidic acid, copper tripeptide-1, adenosine, retinol, and caffeine. Attribution to PDPO is impossible. Structure-activity relationship data from Murad et al. (1992, Archives of Biochemistry and Biophysics) adds an important constraint: replacement of minoxidil's piperidine ring with pyrrolidine abolished lysyl hydroxylase inhibitory activity. This means PDPO likely does not share DPO's collagen-maturation mechanism. Whether K_ATP channel activity is similarly affected by the pyrrolidine substitution remains untested. Additionally, approximately 40% of minoxidil users are non-responders, linked to low SULT1A1 sulfotransferase activity (Goren et al., 2014, Dermatologic Therapy). Whether PDPO requires analogous metabolic activation is completely unknown. The honest framing is this: PDPO is a structurally plausible K_ATP channel opener. Its membership in the pharmacologically active class remains a hypothesis, not an established fact. Product teams should position it as a contributor within combination systems, not as a standalone proven mechanism. DPO (2,4-diaminopyrimidine-3-oxide, CAS 74638-76-9) is the compound more commonly known as aminexil, developed and commercialized by L'Oréal beginning in the late 1980s. Its mechanism has been more directly studied than PDPO's, but it suffers from a different problem: widespread misidentification of its molecular target. The foundational paper by Mahé et al. (1996, Skin Pharmacology) demonstrated that DPO retains strong inhibition of lysyl hydroxylase mRNA expression in vitro, even without the C6 substituent present in minoxidil. The mechanism is transcriptional — DPO reduces lysyl hydroxylase mRNA levels rather than directly inhibiting enzyme catalysis. No Ki or IC₅₀ values have been published. The original work by Murad and Pinnell (1987, Journal of Biological Chemistry) established that minoxidil suppresses lysyl hydroxylase activity in cultured fibroblasts at 25–500 µM, with recovery blocked by actinomycin D, confirming the transcriptional nature of the effect. Lysyl hydroxylase (encoded by PLOD genes) is an Fe²⁺/2-oxoglutarate-dependent dioxygenase that hydroxylates lysine residues in collagen, enabling subsequent cross-link formation. Lysyl oxidase (LOX) is a completely different enzyme — a copper-dependent amine oxidase that catalyzes a later step in cross-linking via allysine formation. These are distinct proteins with distinct substrates, distinct cofactors, and distinct genomic locations. The conflation of "lysyl hydroxylase" with "lysyl oxidase" in marketing materials is not a semantic quibble; it represents a genuine scientific error that undermines credibility with the technical audience these products are being sold to. DPO is listed in EU Annex III (Entry 93) at a maximum concentration of 1.5% in hair care products, based on the SCCNFP opinion of 3 May 2000. The largest published study is Reygagne et al. (2021, Dermatologic Therapy), an international multicenter observational study of 527 subjects using Aminexil Clinical 5 — a multi-ingredient product. Results included an 82% reduction in pull test at day 90 in men (p < 0.01). However, the study was open-label, uncontrolled, and used a multi-ingredient formula, making attribution to DPO alone impossible. Multiple authors were L'Oréal employees. In a mouse model, Jalilzadeh et al. (2024, BioImpacts) reported that 5% kopexil showed significantly higher hair weight, follicle count, anagen percentage, and VEGF/HGF expression compared to 5% minoxidil over 28 days. This is encouraging preclinical data, but animal model results do not automatically translate to human scalp outcomes. No independent, placebo-controlled, DPO-monotherapy human trial with phototrichogram endpoints has been published. OTZ (L-2-oxothiazolidine-4-carboxylic acid, CAS 19771-63-2, MW 147.15) is the best-characterized molecule in this trio from a biochemical standpoint, yet paradoxically the one with the least hair-specific evidence. Williamson and Meister (1981, Proceedings of the National Academy of Sciences) established OTZ as a substrate for 5-oxoprolinase (EC 3.5.2.9), demonstrating that OTZ administration to glutathione-depleted mice restored normal hepatic glutathione levels. They described OTZ as "an intracellular delivery system for cysteine." The mechanism is clean: 5-oxoprolinase cleaves OTZ in an ATP-dependent reaction, yielding an unstable S-carboxycysteine intermediate that spontaneously decarboxylates to L-cysteine and CO₂. Cysteine then enters the two-step glutathione biosynthesis pathway as the rate-limiting substrate. The head-to-head ARDS trial by Bernard et al. (1997, Chest, n=46, randomized, double-blind, placebo-controlled) showed a 49% increase in red blood cell glutathione with intravenous OTZ — comparable to the 47% increase seen with NAC. Oral dosing up to 9 g/day for two years was safe with no significant clinical pathology changes. OTZ has been studied in HIV, ALS, coronary artery disease, and peritoneal dialysis contexts (Moberly et al., 1998, Journal of the American Society of Nephrology). Key advantages over NAC include superior chemical stability, neutral taste and odor, purely intracellular activation (no extracellular thiol reactivity), and better bioavailability. In neonatal toxicity studies, OTZ showed dramatically lower toxicity than equimolar free cysteine — 10% versus 80% mortality at equivalent cysteine-delivering doses. Despite this robust systemic pharmacology, no published peer-reviewed study has examined topical OTZ on human scalp or hair follicle tissue. The mechanistic rationale — cysteine supports keratin synthesis via disulfide cross-links, glutathione provides antioxidant defense against ROS-mediated follicular damage — is sound but unvalidated in the specific tissue context. Jacques et al. (2021, International Journal of Cosmetic Science) demonstrated that OTZ formulated in a sunscreen emulsion was rapidly absorbed through reconstructed human epidermis, providing the most directly relevant evidence for topical OTZ penetration and antioxidant activity in a cosmetic context. This is encouraging for delivery feasibility, but it is not a scalp-specific study. The connection to AGA pathology is indirect but coherent: Shin et al. (2013, BMB Reports) showed that reactive oxygen species mediate androgen-induced TGF-β1 expression in dermal papilla cells. If OTZ can deliver cysteine to follicular tissue and support local glutathione levels, it could theoretically dampen the ROS-TGF-β1 axis. But "theoretically" is the operative word. Responsible product development in this category requires acknowledging specific evidence boundaries: PDPO-specific pharmacological data does not exist in published literature. No electrophysiology, no EC₅₀, no SUR selectivity, no monotherapy clinical trials. DPO's molecular target is lysyl hydroxylase, not lysyl oxidase. Marketing materials that use "LOX inhibitor" language are citing an enzyme that has not been shown to be the target in published peer-reviewed studies. DPO clinical evidence is entirely from multi-ingredient formulations. No independent, controlled, DPO-monotherapy human RCT has been published. OTZ scalp-specific data is absent. The biochemistry is robust; the tissue-specific translation is an open question. Dual-active salt bioavailability has not been directly demonstrated. Whether both the active base and the OTZ counterion reach effective intracellular concentrations from topical application is an evidence gap for both Kopyrrol Aqua and Kopexil Aqua. The three mechanisms map to distinct pathological axes in androgenetic alopecia. K_ATP channel opening (PDPO) addresses the vascular and proliferative axis — vasodilation, VEGF signaling, dermal papilla proliferation. Lysyl hydroxylase inhibition (DPO) addresses the structural and fibrotic axis — reducing collagen cross-linking maturation in the perifollicular environment. Cysteine and glutathione support (OTZ) addresses the oxidative and metabolic axis — ROS scavenging and keratin substrate delivery. This multi-target framing is mechanistically rational. Liu et al. (2025, Nature Reviews Disease Primers) characterize AGA as multifactorial, involving androgen signaling, genetic susceptibility, Wnt pathway modulation, and inflammatory-fibrotic remodeling. A single-mechanism approach is unlikely to address this complexity adequately. However, complementarity between these specific ingredients at cosmetically relevant concentrations and in topical delivery formats has not been experimentally demonstrated. The synergy narrative is a hypothesis, not established fact. Formulators who build programs around this rationale should design studies capable of testing it rather than assuming it. The strongest non-prostaglandin programs being built today share a common characteristic: they separate evidence tiers explicitly in their technical communication. They frame PDPO as a structurally plausible K_ATP-class ingredient with a promising but unvalidated pharmacological profile. They describe DPO's mechanism accurately — as lysyl hydroxylase transcriptional modulation, not LOX inhibition. They present OTZ as a well-characterized cysteine prodrug with systemic proof of concept and plausible topical relevance. This approach is not merely conservative branding. In a regulatory environment where the FDA defines classification by intended use and the EU is actively restricting prostaglandin analogs based on safety evidence gaps, the capacity to make precise, evidence-bounded claims is a structural advantage. It reduces legal risk, accelerates regulatory review, builds trust with sophisticated B2B buyers, and — perhaps most importantly — creates a foundation for genuine clinical substantiation programs that can strengthen claims over time rather than defending overclaims retroactively. The data gaps identified here are not reasons to avoid these ingredients. They are reasons to invest in the specific studies — K_ATP electrophysiology for PDPO, salt-form bioavailability and skin delivery profiling, controlled monotherapy clinical trials — that would move the evidence base from plausible to proven. The market opportunity created by prostaglandin regulatory pressure is real. The question is whether teams will pursue it with the scientific discipline it deserves.

Clinical Result

27 Mar 2026

·www.mironova.com

Perifollicular Fibrosis in AGA: Why the Collagen Axis Deserves More Attention

For decades, the standard narrative around androgenetic alopecia has centered on androgens and the hair follicle cycle: dihydrotestosterone binds androgen receptors in dermal papilla cells, triggers premature catagen entry, and progressively miniaturizes terminal follicles into vellus-like structures. This model is correct as far as it goes. The problem is that it does not go far enough. A growing body of histological evidence shows that the tissue surrounding miniaturizing follicles undergoes significant structural remodeling — and that this remodeling may not be a passive consequence of miniaturization but an active contributor to its persistence. The perifollicular collagen axis, long treated as a footnote in AGA research, is returning to the center of the discussion. Understanding this axis matters for product development because it opens a distinct mechanistic lane — one that ingredients like DPO (diaminopyrimidine oxide, aminexil) are positioned to address. But understanding it also requires confronting the limitations of current evidence and the terminology errors that have accumulated around DPO's mechanism over three decades of commercialization. The histological case for perifollicular fibrosis in AGA rests on several foundational studies. Jaworsky, Kligman, and Murphy (1992, British Journal of Dermatology) characterized inflammatory infiltrates in male pattern alopecia, documenting perifollicular lymphocytic inflammation and collagenous streamers around miniaturizing follicles. Their work established that inflammation and fibrotic change are not incidental findings in AGA scalps but consistent features associated with progressive hair loss. Whiting (1993, Journal of the American Academy of Dermatology) introduced horizontal sectioning of scalp biopsies as a diagnostic methodology and described perifollicular collagenous thickening as a recurring observation in AGA specimens. While Whiting's work focused primarily on the diagnostic value of follicular miniaturization ratios, the fibrotic changes he documented have been cited repeatedly as evidence for matrix remodeling in AGA. More recent work has strengthened rather than weakened this thread. Umar, Tan, and Shitabata (2026, Clinical, Cosmetic and Investigational Dermatology) provide contemporary evidence for perifollicular fibrosis and inflammation as factors in AGA progression, supporting the view that collagen remodeling is not merely historical observation but an active area of investigation with therapeutic implications. Li et al. (2025, Skin Appendage Disorders) published a review framing perifollicular fibrosis explicitly as a modifiable axis in AGA, with collagen cross-linking pathways identified as potential intervention targets. This represents a meaningful shift from the older literature, which tended to describe fibrosis observationally rather than therapeutically. Liu et al. (2025, Nature Reviews Disease Primers) position AGA as a multifactorial condition involving androgen signaling, genetic susceptibility, Wnt pathway modulation, and inflammatory-fibrotic remodeling interactions. The inclusion of fibrotic remodeling as a named axis in a major primer-level review signals that the field has moved beyond treating it as peripheral. The central unresolved question is directionality: does perifollicular fibrosis contribute to miniaturization, or does miniaturization produce fibrosis as a secondary consequence? The honest answer is that the evidence supports both possibilities, and they are not mutually exclusive. The emerging consensus, as framed in contemporary reviews, favors a feedback model: microinflammation triggers TGF-β and Smad-driven myofibroblast activation, which drives collagen deposition and matrix stiffening, which in turn disrupts dermal papilla signaling and impairs follicular cycling. In this model, fibrosis is both consequence and contributor — a vicious cycle rather than a one-directional cause. For product development purposes, the practical implication is clear: whether fibrosis is primary or secondary, reducing perifollicular collagen rigidification is a rational strategy with histological support. The question is whether any available cosmetic ingredient can meaningfully do so. The foundational mechanistic study for DPO is Mahé, Buan, and Bernard (1996, Skin Pharmacology). Using RT-PCR in a structure-activity framework, they demonstrated that 2,4-diaminopyrimidine-3-oxide (aminexil) — the compound lacking the C6 piperidinyl group present in minoxidil — retains strong inhibition of lysyl hydroxylase mRNA expression in vitro. The significance of this finding is that it identified a mechanism for DPO that is independent of K_ATP channel biology. DPO was specifically selected from over 150 pyrimidine N-oxide derivatives because it retained anti-lysyl hydroxylase activity without the vasodilatory and antihypertensive effects associated with minoxidil's channel-opening activity. L'Oréal's original patent (US 4,973,474, filed 1989) covers 2,4-diaminopyrimidine-3-oxide derivatives for hair loss treatment and prevention on this basis. The broader context comes from Murad and Pinnell (1987, Journal of Biological Chemistry), who established that minoxidil suppresses lysyl hydroxylase activity in cultured fibroblasts at concentrations of 25–500 µM. Recovery was blocked by actinomycin D, confirming that the mechanism operates at the transcriptional level — this is mRNA suppression, not direct enzyme inhibition. No Ki or IC₅₀ values have been published for DPO against lysyl hydroxylase protein. Murad et al. (1992, Archives of Biochemistry and Biophysics) extended the SAR analysis, demonstrating that the C6 substituent structure affects which biological activities are retained. The pyrrolidine substitution in PDPO abolished lysyl hydroxylase inhibitory activity, while DPO — lacking any C6 substituent entirely — retained it. This SAR data is important because it shows that the lysyl hydroxylase mechanism is pharmacophore-dependent but separable from the potassium channel mechanism. This is where the terminology problem becomes critical. Lysyl hydroxylase (encoded by PLOD genes) is an Fe²⁺/2-oxoglutarate-dependent dioxygenase that hydroxylates lysine residues in procollagen, a modification required for subsequent stable cross-link formation. Lysyl oxidase (LOX) is a copper-dependent amine oxidase that catalyzes a different reaction — oxidative deamination of lysine and hydroxylysine residues in collagen and elastin to form allysine, enabling covalent cross-linking of mature fibers. These are fundamentally different enzymes. They have different substrates, different cofactors (iron versus copper), different genomic locations, and different positions in the collagen maturation cascade. Lysyl hydroxylase acts on procollagen intracellularly; lysyl oxidase acts on secreted collagen extracellularly. The published peer-reviewed evidence for DPO supports modulation of lysyl hydroxylase mRNA expression. The widespread description of DPO as a "lysyl oxidase inhibitor" in marketing materials, product pages, and even some corporate press materials does not reflect the primary literature. This conflation has persisted for over two decades, and it undermines the scientific credibility of DPO-based claims with the technical audience — dermatologists, formulation scientists, and regulatory reviewers — that matters most for serious product positioning. The SCCNFP (2000) concluded that DPO is "not a derivative of Minoxidil" and that its pharmacological activity is "unknown" — language that reflected the committee's assessment that the mechanism had not been fully characterized by pharmaceutical standards, even if L'Oréal's in-house research had identified the lysyl hydroxylase thread. Perifollicular fibrosis in AGA does not occur in isolation. It connects to the androgen-signaling axis through TGF-β1. Inui et al. (2003, Journal of Investigative Dermatology Symposium Proceedings) identified androgen-inducible TGF-β1 from dermal papilla cells as a key mediator suppressing epithelial growth in AGA. TGF-β1 is both a catagen-promoting signal and a potent pro-fibrotic factor — it drives Smad-dependent transcription of collagen genes, activates myofibroblasts, and promotes extracellular matrix deposition. Shin et al. (2013, BMB Reports) demonstrated that the induction of TGF-β1 by androgens in dermal papilla cells is mediated by reactive oxygen species. This ROS-TGF-β1 link is significant because it connects oxidative stress — a potentially modifiable factor — to the fibrotic cascade. NAC, an antioxidant and cysteine donor mechanistically similar to OTZ, was shown to suppress androgen-inducible TGF-β1 in dermal papilla cells in the same body of work. It is worth noting that TGF-β2, not TGF-β1, appears to be the primary isoform driving catagen induction in human hair follicles (Hibino and Nishiyama, 2004, Journal of Dermatological Science). TGF-β1 knockout mice show delayed catagen (Foitzik et al., 2000, FASEB Journal), confirming the isoform's involvement in follicle regression, but the relative contributions of β1 and β2 in human AGA remain an area of active investigation. The relevance of TGF-β biology to DPO is indirect but meaningful. TGF-β drives fibrosis through the same collagen deposition and maturation cascade that lysyl hydroxylase participates in. If DPO reduces lysyl hydroxylase expression — as the Mahé data supports — it addresses a downstream component of the TGF-β-driven fibrotic program. This creates a rational basis for combination strategies pairing anti-fibrotic (DPO) with antioxidant/GSH-supporting (OTZ) approaches, since they target different points in the same pathological cascade. However, this complementarity is conceptual. No published study has directly tested whether DPO and OTZ produce additive or synergistic effects on perifollicular collagen remodeling or any follicular endpoint. The clinical evidence for DPO is concentrated in product-level studies of multi-ingredient formulations: Reygagne et al. (2021, Dermatologic Therapy): An observational study of 527 subjects using Aminexil Clinical 5, a multi-ingredient product. Pull test reduction of 82% in men at day 90 (p < 0.01). Open-label, no placebo control, multiple L'Oréal-affiliated authors. Piraccini et al. (2011, Giornale Italiano di Dermatologia e Venereologia): Open-label study of aminexil plus arginine. Pull test reduction of 67.7% at 45 days, 82% at 90 days in men. No placebo, multi-ingredient. Jalilzadeh et al. (2024, BioImpacts): Controlled mouse model comparing 5% kopexil versus 5% minoxidil over 28 days. Kopexil showed significantly higher hair weight, follicle count, anagen percentage, and VEGF/HGF expression. Preclinical only. No published, independent, placebo-controlled, DPO-monotherapy human trial with phototrichogram or trichoscopy endpoints has been identified in the peer-reviewed literature. No study has demonstrated histological reversal of perifollicular fibrosis by DPO in human scalp biopsies. These are the evidence gaps that separate DPO's mechanistic rationale from pharmaceutical-grade clinical proof. A Vichy-sponsored RCT (NCT06590779) has been registered but results have not yet been published. Human scalp histology showing DPO-mediated reduction in perifollicular fibrosis has not been published. Lysyl oxidase enzyme kinetics (Ki/IC₅₀) for DPO have not been reported in peer-reviewed literature. Clinical outcomes are from multi-ingredient, sponsor-funded, open-label studies. DPO likely lacks K_ATP channel opening activity based on SAR data (Murad 1992), so combining it with DPO's "anti-fibrotic" positioning and K_ATP-related claims in the same product narrative is problematic unless two distinct active ingredients are being referenced. Competitive benchmarking against minoxidil — which has extensive, independent, controlled clinical evidence — should be framed carefully. For teams building scalp products around the fibrosis axis, this evidence landscape changes study design in three important ways. First, endpoint selection matters. Pull tests and subjective assessments are insufficient to substantiate an anti-fibrotic mechanism. Programs that take this pathway seriously need longer follow-up periods and structure-sensitive endpoints — trichoscopy-derived measures, possibly scalp biopsies with collagen staining in early-phase work. Second, attribution discipline matters. If the product is a multi-ingredient formula, the study should be designed to test the formula, not make claims about individual ingredients that the design cannot support. Alternatively, monotherapy arms can be included specifically to address attribution. Third, terminology accuracy matters. Describing DPO as a "lysyl oxidase inhibitor" when the published evidence supports lysyl hydroxylase transcriptional modulation is not merely imprecise — it is the kind of error that sophisticated buyers, dermatologists, and regulatory reviewers will notice and penalize. The collagen maturation modulation narrative is strong enough on its own merits; it does not need to borrow from a different enzyme. Most competing cosmetic hair actives — Redensyl, Capixyl, Procapil, caffeine, saw palmetto extracts — position around follicle stimulation, DHT reduction, or general antioxidant support. Very few address the perifollicular tissue environment directly. This creates a meaningful differentiation opportunity for products that can credibly claim anti-fibrotic or collagen-maturation-modulating activity. DPO's published evidence, while not pharmaceutical-grade, is specifically relevant to this lane. The Mahé 1996 data — lysyl hydroxylase mRNA suppression in a structure-activity framework — is mechanistically precise enough to survive scrutiny from technical buyers and regulatory reviewers, provided it is communicated accurately (lysyl hydroxylase, not lysyl oxidase; transcriptional modulation, not enzyme kinetics; in vitro, not clinical histological reversal). The broader opportunity is real. Perifollicular fibrosis represents a distinct pathological axis in AGA that is not well addressed by existing cosmetic actives. Products that can credibly position around this mechanism — with accurate science, transparent evidence hierarchy, and commitment to closing the data gaps — will have a structural advantage in a market increasingly demanding scientific rigor.

Clinical Result

28 Nov 2023

·www.prnewswire.com

Navigating the Evolving Market Dynamics of Bone Sarcoma: A Comprehensive Analysis of Osteosarcoma, Ewing Sarcoma, and Chondrosarcoma | DelveInsight

Each individual's risk of being diagnosed with primary bone sarcoma and their chances of recovery following diagnosis are influenced by a range of unique factors. In 2023, it is anticipated that 4K individuals of all ages in the United States will be diagnosed with primary bone sarcoma, including 2K males and 1.8K females. In 2020, approximately 400 cases were reported among those aged 15 to 19. LAS VEGAS, Nov. 28, 2023 /PRNewswire/ -- Bone sarcoma is a rare and aggressive form of cancer that originates in the bone tissue. It poses significant challenges during its treatment due to several factors. Firstly, its rarity often leads to delayed diagnosis, as symptoms can mimic other common conditions. Additionally, bone sarcoma typically affects children and young adults, making the emotional toll of the disease particularly challenging. Treatment often involves a combination of surgery, chemotherapy, and radiation therapy, which can be physically demanding and cause severe side effects. Moreover, because bone sarcoma tends to occur in the extremities, treatment may require complex and lengthy surgical procedures, potentially affecting mobility and quality of life. Furthermore, the risk of recurrence remains a constant concern, necessitating long-term monitoring and follow-up care. Despite these challenges, ongoing research and advancements in medical technology offer hope for improved outcomes and a better quality of life for those battling bone sarcoma. DelveInsight has recently released a series of epidemiology-based market reports focusing on benign bone sarcoma including Osteosarcoma Market Report, Ewing Sarcoma Market Report, and Chondrosarcoma Market Report. These reports include a comprehensive understanding of current treatment practices, historical and forecasted patient pool, emerging drugs, market share of individual therapies, and historical and forecasted market size from 2019 to 2032 segmented into 7MM [the United States, the EU-4 (Italy, Spain, France, and Germany), the United Kingdom, and Japan]. Additionally, the reports feature exhaustive analysis of prominent companies working with their emerging candidates in different stages of clinical development. Let's deep dive into the assessment of these bone sarcoma markets individually. Osteosarcoma Market Osteosarcoma is a rare bone tumor affecting having an annual incidence of 3.4 cases per million. It is the most prevalent form of bone cancer, primarily developed in the osteoblast cells of bones, with a predilection for long bones near the knee joint. However, it can also manifest in other locations, including the upper leg, lower leg, upper arm, and virtually any bone in the body, including those in the pelvis, shoulder, and skull. It has the potential to invade adjacent tissues, such as tendons and muscles, and can metastasize to distant organs or other bones via the bloodstream. As per DelveInsight analysts, the total incident population of osteosarcoma in the 7MM was ~2K in 2022. The estimates show the highest incident cases of osteosarcoma in the United States with ~1K cases in 2022, and it is expected to increase by 2032. Osteosarcoma is commonly treated through a combination of chemotherapy, surgery, and radiation therapy. Despite some recent developments, limited progress has been achieved since the late 1980s when chemotherapy was added to surgical treatment, leading to improved survival rates. Radiation therapy impacts both normal and cancerous cells, causing various effects. Chemotherapeutic drugs like cisplatin, doxorubicin, ifosfamide, and high-dose methotrexate with leucovorin calcium rescue (HDMTX) are widely used. Additionally, a few FDA-approved products, such as FUSILEV and KHAPZORY, are available for osteosarcoma treatment. As per DelveInsight analysis, the osteosarcoma market size is expected to increase at a significant CAGR by 2032. This growth would be fuelled by the increase in the patient pool and the expected entry of emerging therapies. Osteosarcoma Pipeline Therapies and Companies Lenvatinib: Eisai Naxitamab: Y-mAbs Therapeutics BAY80-6946: Bayer Vactosertib: MedPacto For a comprehensive view of the osteosarcoma market, check out the Osteosarcoma Market Assessment Ewing Sarcoma Market Ewing Sarcoma, a malignant tumor, typically initiates its growth within the bones, with a higher incidence among children and young adults, often manifesting during adolescence. Although it can originate in any bone, it predominantly affects the long bones, such as the thigh bone, shin bone, and upper arm bone. The pelvis bones are also frequently involved. In some cases, the tumor may originate in muscle and soft tissues. Common symptoms include bone stiffness, pain, swelling, or tenderness, along with tissue surrounding the affected bone. As per the assessment done by DelveInsight, the total incident cases of Ewing sarcoma in the 7MM comprised approximately 1.2K cases in 2022 and are projected to increase during the forecasted period. The management of Ewing sarcoma typically adopts a comprehensive approach, which may encompass surgery, chemotherapy, and radiation therapy. The National Comprehensive Cancer Network (NCCN) offers specific chemotherapy regimens for localized and metastatic Ewing sarcoma. For first-line treatment, NCCN suggests VDC/IE (vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide), VAIA (vincristine, doxorubicin, ifosfamide, and dactinomycin), and VIDE (vincristine, ifosfamide, doxorubicin, and etoposide) for both initial presentations and as primary therapy for metastatic disease. In the second-line setting, NCCN recommends options like Cyclophosphamide and topotecan, Irinotecan + temozolomide ± Vincristine, Ifosfamide, carboplatin, etoposide, and Lurbinectedin. As per the latest Ewing Sarcoma Market Report, the total Ewing sarcoma market size in the 7MM is approximately USD 26 million in 2022 and is projected to increase during the forecast period (2023–2032). The expected introduction of upcoming therapies and the deepened integration of early patient screening, medication management in secondary care, and diverse clinical setups, ongoing research into optimal implementation approaches, and a surge in public awareness will ultimately pave the way for the advancement of efficient treatment choices. Ewing Sarcoma Pipeline Therapies and Companies SECLIDEMSTAT (SP-2577): Salarius Pharmaceuticals ZEPZELCA (LURBINECTEDIN): Jazz Pharmaceuticals and PharmaMar VERZENIO (ABEMACICLIB): Eli Lilly IBRANCE (PALBOCICLIB): Pfizer MECBOTAMAB VEDOTIN (BA3011): Bioatla IOPOFOSINE I 131 (CLR 131): Cellectar Biosciences TP-1287: Sumitomo Pharma Oncology NBRX-109: Inhibrx Explore in-depth for a comprehensive understanding of the Ewing Sarcoma Clinical Trials Chondrosarcoma Market Chondrosarcoma comprises a group of bone tumors originating from cells that overproduce cartilage. Among these tumors, conventional chondrosarcoma is the most frequent type and is generally associated with slow growth. Conversely, rarer subtypes like dedifferentiated chondrosarcoma, myxoid chondrosarcoma, clear cell chondrosarcoma, and mesenchymal chondrosarcoma tend to exhibit a more aggressive growth pattern and have the potential to spread to distant body parts. DelveInsight estimated that the total incident cases of chondrosarcoma in the 7MM comprised approximately 2K cases in 2022 and are projected to increase during the forecasted period. The management approach for chondrosarcoma is contingent upon factors like tumor type, grade, and location, with the grading system serving as the most reliable indicator of clinical prognosis. It is firmly established that surgical intervention remains the gold standard and sole effective treatment for chondrosarcoma, as alternative modalities such as radiotherapy and chemotherapy exhibit limited responsiveness and resistance. Surgical options encompass curettage, radical resection, and amputation, each necessitating comprehensive clinical judgment and contingent upon variables such as lesion size, location, and malignant characteristics. Anticipated advancements in upcoming therapies and increased integration of early patient screening and medication within secondary care and other clinical settings, along with ongoing research to determine the best implementation methods, are expected to contribute to the development of more effective treatment options. However, chondrosarcoma, being an orphan disease, presents challenges in conducting clinical trials. Limited outcome data for locally advanced or metastatic patients underscore the need for new treatment approaches. Phase I trials, due to their small number of chondrosarcoma patients at varying dose levels, make it difficult to draw definitive conclusions. Nevertheless, some Phase II trials have yielded promising results, warranting further investigation. Encouraging retrospective studies could help augment the currently limited data. Urgent efforts to boost research studies on this orphan disease are imperative. As per DelveInsight analysis, the total market size of chondrosarcoma in the 7MM is approximately USD 9 million in 2022 and is projected to increase at a massive CAGR of 24.8% due to increasing awareness of the disease and the launch of the emerging therapy. Chondrosarcoma Pipeline Therapies and Companies INBRX-109: Inhibrx To access a complete analysis of the chondrosarcoma market, visit Chondrosarcoma Market Assessment Trending Oncology Reports Non-Small Cell Lung Cancer Market Non-Small Cell Lung Cancer Market Insights, Epidemiology, and Market Forecast – 2032 report delivers an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key NSCLC companies, including EMD Serono, Merck, Cellular Biomedicine Group, Inc., Celgene, CellSight Technologies, Inc., BeyondSpring Pharmaceuticals Inc., J Ints Bio, Forward Pharmaceuticals Co., Ltd., AstraZeneca, Bristol-Myers Squibb, Teligene US, Rain Oncology Inc, ReHeva Biosciences, Inc., Amgen, Novartis, RedCloud Bio, Parexel, Vitrac Therapeutics, LLC, Mythic Therapeutics, Instil Bio, Mirati Therapeutics Inc., Daiichi Sankyo, Inc., AstraZeneca, Precision Biologics, Inc, Promontory Therapeutics Inc., Palobiofarma SL, Regeneron Pharmaceuticals, Revolution Medicines, Inc., Cullinan Oncology, LLC, Iovance Biotherapeutics, Inc., Innate Pharma, among others. Non-Hodgkin Lymphoma Market Non-Hodgkin Lymphoma Market Insights, Epidemiology, and Market Forecast – 2032 report delivers an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key NHL companies, including GAbbVie, Genmab, Novartis, Angiocrine Bioscience, Autolus, Zentera Therapeutics, Jiangsu Hengrui Medicine, among others. Oncolytic Virus Cancer Therapies Market Oncolytic Virus Cancer Therapies Market Insights, Epidemiology, and Market Forecast – 2032 report delivers an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key oncolytic virus cancer therapies companies, including Targovax, Replimune, Genelux Corporation, Candel Therapeutics, DNAtrix, SillaJen, Treovir, Lokon Pharma AB, Istari Oncology, CG Oncology, Amgen, Daiichi Sankyo, among others. Multiple Myeloma Market Multiple Myeloma Market Insights, Epidemiology, and Market Forecast – 2032 report delivers an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key multiple myeloma companies, including Johnson & Johnson (Janssen), Pfizer, AbbVie and Roche (Genentech), Regeneron Pharmaceuticals, Bristol-Myers Squibb, Celgene, Roche (Genentech), Arcellx, Novartis, Regeneron Pharmaceuticals, BeiGene, CARsgen Therapeutics, Cartesian Therapeutics, C4 Therapeutics, Heidelberg Pharma, Bristol-Myers Squibb, RAPA Therapeutics, AbbVie (TeneoOne), Takeda, among others. Oncology Conference Coverage Services DelveInsight's Oncology Conference Coverage Services deliver a comprehensive examination of conference outcomes from a range of prominent events, such as ASCO, ESMO, ASH, AACR, ASTRO, SOHO, SITC, European CAR T-cell Meeting, and IASLC 2023. This in-depth analysis equips businesses with the insights they need for effective competitive intelligence and forecasting market trends, aiding in the development of future strategies. About DelveInsight DelveInsight is a leading healthcare-focused market research and consulting firm that provides clients with high-quality market intelligence and analysis to support informed business decisions. With a team of experienced industry experts and a deep understanding of the life sciences and healthcare sectors, we offer customized research solutions and insights to clients across the globe. Get hassle-free access to all the healthcare and pharma market research reports through our subscription-based platform PharmDelve . Contact Us Shruti Thakur [email protected] +1(919)321-6187 Logo: SOURCE DelveInsight Business Research, LLP

Phase 2Clinical ResultRadiation TherapyASCO

100 Deals associated with Dactinomycin

External Link

KEGG	Wiki	ATC	Drug Bank
D00214	Dactinomycin	L01DA01	DB00970

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Hodgkin's Lymphoma	China	Shaanxi Wuzhou Pharmaceutical Co Ltd	01 Jan 1995
Neuroblastoma	China	Shaanxi Wuzhou Pharmaceutical Co Ltd	01 Jan 1995
Choriocarcinoma	Japan	Nobelpharma Co., Ltd.	16 Dec 1968
Ewing Sarcoma	United States	Recordati Rare Diseases, Inc.	10 Dec 1964
Gestational Trophoblastic Disease	United States	Recordati Rare Diseases, Inc.	10 Dec 1964
Local Neoplasm Recurrence	United States	Recordati Rare Diseases, Inc.	10 Dec 1964
Rhabdomyosarcoma	United States	Recordati Rare Diseases, Inc.	10 Dec 1964
Testicular Neoplasms	United States	Recordati Rare Diseases, Inc.	10 Dec 1964
Wilms Tumor	United States	Recordati Rare Diseases, Inc.	10 Dec 1964

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Acute Myeloid Leukemia	Phase 2	Italy	Actavia Life Sciences, Inc.	-

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESGO2026	Not Applicable	Gestational Trophoblastic Disease	106	Methotrexate	mrbwxvullp(ttbhjxxdbt) = cbqdlhtbgs buxswlirrb (axgnivehwv ) View more	Positive	28 Feb 2026
				EMA-CO regimen - Etoposide, Methotrexate, Actinomycin-D, Cyclophosphamide and Vincristine	gbngcdrrag(puzdmvgigl) = cycakpfxfx hmqmsswndi (csjrdnycfy, 12 - 66)
NCT04562558 (Pubmed \| Ann Oncol)	Not Applicable	Gestational Trophoblastic Disease First line	228	Actinomycin D	kxiujtrrtt(gmdkommpvx) = nprfgfmdpc dqdiogubdv (ndawinnhwl ) View more	Positive	01 Oct 2025
				Methotrexate-folinic acid	kxiujtrrtt(gmdkommpvx) = lghecrdfvm dqdiogubdv (ndawinnhwl ) View more
NCT00047138 (SIOP WT 2001 Study, Pubmed)	Phase 3	Wilms Tumor Neoadjuvant \| Adjuvant	-	Dactinomycin and Vincristine (AV)	ctsujfuyez(aqtrbrddxo) = pvkvhlnlww sbdpdaijrf (edtacwbnst ) View more	Positive	30 Jul 2024
SOHO2023	Not Applicable	-	-	Venetoclax + low-dose cytarabine + actinomycin D	ouqtpnnxtz(oegfuqftqn) = 11% akhfcaayqv (atjribjrwu ) View more	-	01 Sep 2023
NCT00945009 (AREN0534, Pubmed \| Ann Surg Oncol)	Phase 3	Urologic Neoplasms	9	Vincristine and Dactinomycin (regimen EE4A)	suubuswngr(raaynnizjq) = ceyyftgvbl jfcakqclkh (cetezhwdas ) View more	Positive	01 May 2022
NCT01535053 (NRG/GOG 275, Pubmed \| Gynecol Oncol)	Phase 3	Gestational Trophoblastic Disease	57	Pulse actinomycin-D	hwsbkossiu(tzisiwoode) = ykymstjeiz djjcdourtf (ixggvttcah )	Positive	01 Aug 2020
				Multi-day methotrexate	hwsbkossiu(tzisiwoode) = tahphfvhno djjcdourtf (ixggvttcah )
ASCO2020	Not Applicable	Ewing Sarcoma First line	-	VAIA combination	cvgprzsojk(nswiomwomw) = lxluyrpaew odwfjlgjar (seffhjrixv )	Negative	25 May 2020
NCT01014767 (CPT-SIOP-2009, CTgov)	Phase 3	Choroid Plexus Papilloma \| Choroid Plexus Carcinoma \| Choroid Plexus Neoplasms ... View more	27	Etoposide+Cyclophosphamide+Carboplatin+Vincristine (Standard Arm (1))	syelwqpvig(vjoqsjmven) = pdsutoznvq jiviclzvxi (xoekysoqrg, nkuhvkrtqr - bokmnsvwsm) View more	-	20 Aug 2019
				Etoposide+Cyclophosphamide+Carboplatin+Doxorubicin+Dactinomycin+cisplatin+Vincristine (Doxorubicin/Cisplatin Arm (2))	syelwqpvig(vjoqsjmven) = hagoxcvjxb jiviclzvxi (xoekysoqrg, gkatktoefi - nvvluylkeg) View more
NCT01535053 (NRG/GOG 275, CTgov)	Phase 3	Hydatidiform Mole \| Choriocarcinoma	57	Dactinomycin (Regimen I (Dactinomycin))	wntbmbkkwk = trhrtocctv ccsosfqsvn (sgewsfzpyz, xlvubuzgvv - jwtuswhfvm) View more	-	13 Aug 2019
				Methotrexate (Regimen II (Methotrexate))	wntbmbkkwk = nbgwdaxutu ccsosfqsvn (sgewsfzpyz, jymratdlfr - agylfyuzoe) View more
EHA2019	Not Applicable	Refractory acute myeloid leukemia	19	Venetoclax + Low dose cytarabine	qtvtkvcgpl(livnmqfmsn) = sepsis (5/19, 26%), pneumonia (5/19, 26%), catheter related infections (3/19, 16%) and febrile neutropenia (3/19, 16%) cclsmhbhdr (wrmofyfbnx ) View more	-	14 Jun 2019

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