RARE DISEASE
Dihydropyrimidine dehydrogenase deficiency
Dihydropyrimidine dehydrogenase deficiency
Dihydropyrimidine dehydrogenase deficiency
Synonyms: Familial pyrimidinemia
Synonyms: Familial pyrimidinemia
Synonyms: Familial pyrimidinemia
Drug discovery
1
drug
With orphan designation
Overview
Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder impairing pyrimidine metabolism due to DPYD gene mutations. It causes toxic accumulation of thymine/uracil and severe fluoropyrimidine (5-FU/capecitabine) toxicity due to reduced drug detoxification. Clinical manifestations range from asymptomatic carriers to neurodevelopmental delays, seizures, and microcephaly in severe cases [1][2][6]. Pre-treatment screening is critical to mitigate life-threatening adverse drug reactions [6][13].
Therapies
Categories: rare genetic diseases, rare inborn errors of metabolism
Research Papers
235 drug discovery papers about Dihydropyrimidine dehydrogenase deficiency, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
235 drug discovery papers about Dihydropyrimidine dehydrogenase deficiency, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
2026-05-28 | NGS-based DPYD diplotype analysis beyond conventional targeted variant testing in an ethnically diverse cancer patient cohort.
e15131 Background: Germline variants in the highly polymorphic DPYD gene are the main cause of dihydropyrimidine dehydrogenase (DPD) deficiency and are strongly associated with fluoropyrimidine-related toxicity. PCR-based assays test limited predefined variants and may miss clinically relevant alleles, particularly in ethnically diverse populations. Next-generation sequencing (NGS) allows broader and comprehensive assessment of DPYD variation. Methods: This retrospective study included 4,380 diagnosed cancer patients of Caucasian and non-Caucasian ancestry undergoing routine DPYD testing using NGS-based profiling with the Shield assay at Datar Cancer Genetics. Identified variants were translated into diplotypes and assigned activity scores according to CPIC and DPWG guidelines, classifying patients as normal, intermediate, or poor metabolizers. Results: Clinically relevant DPYD variants associated with reduced or absent DPD activity were identified in 4.8% (211/4380) of patients, comprising 4.7% (n = 209) intermediate and 0.1% (n = 2) poor metabolizers. Reduced-function and no-function alleles detected in the cohort included *2A, HapB3, and c.557A>G, either in heterozygous or compound diplotype configurations. Intermediate metabolizer status was driven by diplotypes such as *9A/HapB3 and c.557A>G–containing combinations, reflecting the impact of a single reduced-function allele when paired with an otherwise normal allele. Poor metabolizer phenotypes were exclusively associated with biallelic or compound heterozygous diplotypes involving known no-function or severely reduced-function alleles, including *2A/*2A and HapB3/*2A. Notably, several clinically actionable diplotypes would not have been detected by assays limited to a small set of predefined variants, emphasizing the importance of comprehensive NGS-based DPYD profiling and diplotype-level interpretation for accurate phenotype assignment. Conclusions: Nearly 5% of patients were classified as intermediate or poor metabolizers, placing them at increased risk for severe fluoropyrimidine toxicity. Comprehensive NGS-based DPYD testing enables detection of both common and rare reduced-function variants, supports more accurate phenotype assignment, and provides a practical approach to safer fluoropyrimidine dosing in ethnically diverse clinical populations. Clinically actionable DPYD alleles identified by NGS. Allele Frequency Function HapB3 3.04% Reduced function allele *2A 0.91% Absent DPYD activity allele c.2846A>T 0.50% Reduced function allele c.2279C>T 0.23% Reduced function allele c.557A>G 0.11% Reduced function allele *4 3.45% Absent DPYD activity allele *13 0.07% Absent DPYD activity allele *3 0.02% Absent DPYD activity allele *8 0.02% Absent DPYD activity allele
2026-05-23 | Dihydropyrimidine dehydrogenase phenotype-guided dose individualization of fluoropyrimidine in gastrointestinal cancers: PRODIGE100-UCGI48-FUDOSE phase II study.
Pre-treatment screening for dihydropyrimidine dehydrogenase (DPD) deficiency based on plasma uracil concentration ([U]) is mandatory in France before fluoropyrimidine (FP) administration. However, dose-adjustment strategies according to [U] in case of partial DPD deficiency remain empirical, heterogeneous across centers and lacking clear recommendations. This national, multicenter, open-label phase II trial will enroll approximately 400 patients schedule to receive FP-based chemotherapy combined with oxaliplatin, with or without targeted therapy. Patients will be stratified by pre-treatment [U] into one control arm (non-DPD-deficient, [U] <16 ng/mL) receiving a full standard FP starting dose, and four DPD-deficient cohorts ([16-20[, [20-50[, [50-100[, and [100-150[ ng/mL) receiving prespecified starting dose. The primary endpoint is FP-induced grade ≥3 hematological and gastrointestinal toxicity during the first two treatment cycles, compared between DPD-deficient cohorts vs control arm within a Bayesian framework. Interim analyses with sequential toxicity monitoring are planned to allow protocol adaptation if safety concerns arise. Secondary endpoints include overall toxicity profiles, dose adaptations, survival outcomes, pharmacokinetic analyses, and correlations between [U] levels and DPYD genotypes. This trial addresses a major gap between mandatory preemptive DPD phenotyping and actionable FP dosing recommendations, to generate prospective evidence supporting safer and harmonized FP use in routine clinical practice. FUDOSE is registered at Clinicaltrials.gov (NCT06475352).
2026-05-03 | Dabupi decoction mitigates fluorouracil-induced intestinal mucositis via farnesoid X receptor activation and dihydropyrimidine dehydrogenase upregulation.
5-Fluorouracil (5-FU) is a widely utilized antimetabolite in colorectal cancer chemotherapy, primarily exerting its cytotoxic effects by irreversibly inhibiting thymidylate synthase (TS). This inhibition leads to a reduction in deoxythymidine monophosphate (dTMP), which disrupts DNA synthesis and repair. A major challenge in 5-FU treatment is the dose-limiting toxicity of chemotherapeutic-induced intestinal mucositis. Da-Bu-Pi Decoction (DBPD), a well-established formula in traditional Chinese medicine for treating spleen-stomach deficiency, is often used to enhance spleen qi and balance the middle jiao. While growing clinical evidence points to the therapeutic benefits of DBPD in alleviating 5-FU-induced mucositis, the underlying molecular mechanisms remain largely undefined. To elucidate the molecular mechanisms underlying chemotherapy-induced intestinal mucositis (CIM) induced by 5-FU, with a focus on the disruption of bile acid metabolism and the downregulation of the key detoxifying enzyme DPYD expression. DBPD was administered orally to C57BL/6 mice with 5-FU-induced intestinal mucositis over a seven-day period. The evaluation of intestinal damage included assessments of diarrhea, morphology, intestinal barrier function and inflammatory factors, alongside techniques such as immunofluorescence, immunohistochemistry, transmission electron microscopy and Western blot. Transcriptome analysis of mouse ileal tissue was applied to reveal differentially expressed genes (DEGs) in different treated mice, and bile acid metabolism-related genes (UDP-glucuronosyltransferase 1A1 (UGT1A1), UGT1A9, Farnesoid x receptor (FXR), TGR5) and DPYD, a key detoxification enzyme for 5-FU, were confirmed by qRT-PCR. Additionally, changes of DCA and LCA were measured using ELISA. Bioinformatics helped delineate the association of these genes with pan-cancer versus normal tissues. Meanwhile, 5-FU-induced intestinal epithelial cells (HIEC) were treated with serum containing DBPD. It was further explored how DBPD modulates the UGT1A1/TGR5/FXR signaling pathway and enhances DPYD activity to reduce apoptosis and intestinal barrier damage in 5-FU induced HIEC. AlphaFold3 and further bioinformatics analysis predicted the binding interactions and expression correlations among UGT1A1, UGT1A9 and FXR. DBPD is protective by reducing inflammation and intestinal barrier dysfunction in 5-FU-induced intestinal mucositis. Transcriptome analysis and in vivo validation highlighted the crucial function of bile acid metabolism-related pathways and DPYD in 5-FU-induced CIM. 5-FU increased the levels of deoxycholic acid (DCA) and lithocholic acid (LCA) in the mouse ileum. DBPD activated the UGT1A1/TGR5/FXR pathway and up-regulated DPYD to suppress the pathological accumulation of these specific cytotoxic bile acids within the local intestinal microenvironment and ameliorate 5-FU-induced CIM. It was indicated by the analysis of bioinformatics that low levels of UGT1A1, UGT1A9, and FXR exhibited a connection with poor prognosis within colorectal cancer. In vitro studies confirmed that DBPD significantly improved the UGT1A1/TGR5/FXR pathway and increased the expression of DPYD in 5-FU treated HIEC, thereby improving intestinal barrier integrity and alleviating apoptosis. Further validation using the FXR inhibitor (Gly-β-MCA) showed that DBPD ameliorated Gly-β-MCA induced HIEC apoptosis and barrier attenuation. Finally, AlphaFold3 and bioinformatics predictions suggested potential binding interactions between UGT1A1, UGT1A9 and FXR with positively correlated expression.
2026-03-09 | DPYD genotyping in patients receiving capecitabine: an exploratory analysis from the D-TORCH study.
Introduction: Deficiency of the dihydropyrimidine dehydrogenase enzyme can result in capecitabine-related toxicity due to genetic alterations in the DPYD gene, leading to complete or partial DPD deficiency and poor or intermediate metabolizer phenotypes. The distribution of DPYD variants varies across populations. While routine DPYD genotyping is recommended in Western populations, data from India, particularly from next-generation sequencing (NGS)-based studies, remain limited. Methods: This exploratory analysis was conducted within the D-TORCH trial, a randomized, double-blind, placebo-controlled study evaluating topical diclofenac for prevention of capecitabine-induced hand-foot syndrome. Germline whole-exome sequencing was performed in consenting patients prior to capecitabine initiation. DPYD variants were identified using an NGS pipeline, annotated via ANNOVAR and PharmGKB, and classified according to CPIC guidelines. Results: Seventy-six patients underwent DPYD sequencing; 54 (71%) carried at least one variant and 22 (29%) were wild-type. Thirteen coding or splice-site variants were identified, including three (3.9%) associated with an intermediate metabolizer phenotype; no poor metabolizers were detected. The most common variants were classified as normal metabolizers. Grade 2 toxicity occurred in 63.6% of variant carriers and 55.6% of wild-type patients, with diarrhea and mucositis being most frequent. No significant association was observed between DPYD variant status and toxicity. Discussion: This first NGS-based DPYD report from India highlights the low prevalence of clinically actionable variants. Larger studies are required to validate these findings and guide population-specific fluoropyrimidine dosing strategies.
2026-02-06 | Results of a phase II trial of short-course radiation and TASOX [trifluridine/tipiracil (TAS-102) plus oxaliplatin] chemotherapy in operable rectal cancer.
Trifluridine/tipiracil (FTD/TPI) is approved for metastatic colorectal cancer as monotherapy or in combination with bevacizumab, though dosing in combination with oxaliplatin has not yet been established. The objective of the phase II SHORT trial (NCT04417699) was to determine the efficacy of short-course radiation (SC RT) followed by 3 months of FTD/TPI + oxaliplatin (TASOX) as a condensed total neoadjuvant therapy (TNT) regimen for intermediate-risk rectal cancer. Eligible patients with clinical T3N0 or T1-3N1 nonlow rectal tumors and negative radial tumor margins (>1 mm) were enrolled. The primary endpoint was reduction in neoadjuvant response (NAR) score compared with historic controls. Patients received 25 Gy in five 5 Gy fractions of conformal pelvic radiation followed by six planned 14-day cycles of TASOX: FTD/TPI (35 mg/m2/dose) orally b.i.d. day 1-5, oxaliplatin 85 mg/m2 i.v. day 1. Surgery was recommended within 4 weeks after cycle 6 of TASOX. Between 2020 and 2023, 13 patients with stage II (n = 5) and III (n = 8) rectal adenocarcinoma were enrolled at three institutions. Dose delivered was 100% of planned radiation, 99% of planned FTD/TPI and 95% oxaliplatin. Diarrhea was documented with a frequency of 11%, and was grade 1 only. Only 9% (8/87) of adverse events were grade 3/4, predominantly related to neutropenia. Among 10 patients who proceeded to total mesorectal excision surgery, 2 experienced a pathological complete response and 2 had a complete clinical response, of which 1 had no evidence of regrowth on continued watch and wait. SC RT and 3 months of TASOX can be safely delivered to patients with intermediate-risk rectal cancer, offering a convenient regimen that should be further explored for rectal cancer treatment. The TASOX regimen may be of particular relevance for patients with suspected dihydropyrimidine dehydrogenase deficiency who require oxaliplatin-based therapy.
2026-05-28 | NGS-based DPYD diplotype analysis beyond conventional targeted variant testing in an ethnically diverse cancer patient cohort.
e15131 Background: Germline variants in the highly polymorphic DPYD gene are the main cause of dihydropyrimidine dehydrogenase (DPD) deficiency and are strongly associated with fluoropyrimidine-related toxicity. PCR-based assays test limited predefined variants and may miss clinically relevant alleles, particularly in ethnically diverse populations. Next-generation sequencing (NGS) allows broader and comprehensive assessment of DPYD variation. Methods: This retrospective study included 4,380 diagnosed cancer patients of Caucasian and non-Caucasian ancestry undergoing routine DPYD testing using NGS-based profiling with the Shield assay at Datar Cancer Genetics. Identified variants were translated into diplotypes and assigned activity scores according to CPIC and DPWG guidelines, classifying patients as normal, intermediate, or poor metabolizers. Results: Clinically relevant DPYD variants associated with reduced or absent DPD activity were identified in 4.8% (211/4380) of patients, comprising 4.7% (n = 209) intermediate and 0.1% (n = 2) poor metabolizers. Reduced-function and no-function alleles detected in the cohort included *2A, HapB3, and c.557A>G, either in heterozygous or compound diplotype configurations. Intermediate metabolizer status was driven by diplotypes such as *9A/HapB3 and c.557A>G–containing combinations, reflecting the impact of a single reduced-function allele when paired with an otherwise normal allele. Poor metabolizer phenotypes were exclusively associated with biallelic or compound heterozygous diplotypes involving known no-function or severely reduced-function alleles, including *2A/*2A and HapB3/*2A. Notably, several clinically actionable diplotypes would not have been detected by assays limited to a small set of predefined variants, emphasizing the importance of comprehensive NGS-based DPYD profiling and diplotype-level interpretation for accurate phenotype assignment. Conclusions: Nearly 5% of patients were classified as intermediate or poor metabolizers, placing them at increased risk for severe fluoropyrimidine toxicity. Comprehensive NGS-based DPYD testing enables detection of both common and rare reduced-function variants, supports more accurate phenotype assignment, and provides a practical approach to safer fluoropyrimidine dosing in ethnically diverse clinical populations. Clinically actionable DPYD alleles identified by NGS. Allele Frequency Function HapB3 3.04% Reduced function allele *2A 0.91% Absent DPYD activity allele c.2846A>T 0.50% Reduced function allele c.2279C>T 0.23% Reduced function allele c.557A>G 0.11% Reduced function allele *4 3.45% Absent DPYD activity allele *13 0.07% Absent DPYD activity allele *3 0.02% Absent DPYD activity allele *8 0.02% Absent DPYD activity allele
2026-05-23 | Dihydropyrimidine dehydrogenase phenotype-guided dose individualization of fluoropyrimidine in gastrointestinal cancers: PRODIGE100-UCGI48-FUDOSE phase II study.
Pre-treatment screening for dihydropyrimidine dehydrogenase (DPD) deficiency based on plasma uracil concentration ([U]) is mandatory in France before fluoropyrimidine (FP) administration. However, dose-adjustment strategies according to [U] in case of partial DPD deficiency remain empirical, heterogeneous across centers and lacking clear recommendations. This national, multicenter, open-label phase II trial will enroll approximately 400 patients schedule to receive FP-based chemotherapy combined with oxaliplatin, with or without targeted therapy. Patients will be stratified by pre-treatment [U] into one control arm (non-DPD-deficient, [U] <16 ng/mL) receiving a full standard FP starting dose, and four DPD-deficient cohorts ([16-20[, [20-50[, [50-100[, and [100-150[ ng/mL) receiving prespecified starting dose. The primary endpoint is FP-induced grade ≥3 hematological and gastrointestinal toxicity during the first two treatment cycles, compared between DPD-deficient cohorts vs control arm within a Bayesian framework. Interim analyses with sequential toxicity monitoring are planned to allow protocol adaptation if safety concerns arise. Secondary endpoints include overall toxicity profiles, dose adaptations, survival outcomes, pharmacokinetic analyses, and correlations between [U] levels and DPYD genotypes. This trial addresses a major gap between mandatory preemptive DPD phenotyping and actionable FP dosing recommendations, to generate prospective evidence supporting safer and harmonized FP use in routine clinical practice. FUDOSE is registered at Clinicaltrials.gov (NCT06475352).
2026-05-03 | Dabupi decoction mitigates fluorouracil-induced intestinal mucositis via farnesoid X receptor activation and dihydropyrimidine dehydrogenase upregulation.
5-Fluorouracil (5-FU) is a widely utilized antimetabolite in colorectal cancer chemotherapy, primarily exerting its cytotoxic effects by irreversibly inhibiting thymidylate synthase (TS). This inhibition leads to a reduction in deoxythymidine monophosphate (dTMP), which disrupts DNA synthesis and repair. A major challenge in 5-FU treatment is the dose-limiting toxicity of chemotherapeutic-induced intestinal mucositis. Da-Bu-Pi Decoction (DBPD), a well-established formula in traditional Chinese medicine for treating spleen-stomach deficiency, is often used to enhance spleen qi and balance the middle jiao. While growing clinical evidence points to the therapeutic benefits of DBPD in alleviating 5-FU-induced mucositis, the underlying molecular mechanisms remain largely undefined. To elucidate the molecular mechanisms underlying chemotherapy-induced intestinal mucositis (CIM) induced by 5-FU, with a focus on the disruption of bile acid metabolism and the downregulation of the key detoxifying enzyme DPYD expression. DBPD was administered orally to C57BL/6 mice with 5-FU-induced intestinal mucositis over a seven-day period. The evaluation of intestinal damage included assessments of diarrhea, morphology, intestinal barrier function and inflammatory factors, alongside techniques such as immunofluorescence, immunohistochemistry, transmission electron microscopy and Western blot. Transcriptome analysis of mouse ileal tissue was applied to reveal differentially expressed genes (DEGs) in different treated mice, and bile acid metabolism-related genes (UDP-glucuronosyltransferase 1A1 (UGT1A1), UGT1A9, Farnesoid x receptor (FXR), TGR5) and DPYD, a key detoxification enzyme for 5-FU, were confirmed by qRT-PCR. Additionally, changes of DCA and LCA were measured using ELISA. Bioinformatics helped delineate the association of these genes with pan-cancer versus normal tissues. Meanwhile, 5-FU-induced intestinal epithelial cells (HIEC) were treated with serum containing DBPD. It was further explored how DBPD modulates the UGT1A1/TGR5/FXR signaling pathway and enhances DPYD activity to reduce apoptosis and intestinal barrier damage in 5-FU induced HIEC. AlphaFold3 and further bioinformatics analysis predicted the binding interactions and expression correlations among UGT1A1, UGT1A9 and FXR. DBPD is protective by reducing inflammation and intestinal barrier dysfunction in 5-FU-induced intestinal mucositis. Transcriptome analysis and in vivo validation highlighted the crucial function of bile acid metabolism-related pathways and DPYD in 5-FU-induced CIM. 5-FU increased the levels of deoxycholic acid (DCA) and lithocholic acid (LCA) in the mouse ileum. DBPD activated the UGT1A1/TGR5/FXR pathway and up-regulated DPYD to suppress the pathological accumulation of these specific cytotoxic bile acids within the local intestinal microenvironment and ameliorate 5-FU-induced CIM. It was indicated by the analysis of bioinformatics that low levels of UGT1A1, UGT1A9, and FXR exhibited a connection with poor prognosis within colorectal cancer. In vitro studies confirmed that DBPD significantly improved the UGT1A1/TGR5/FXR pathway and increased the expression of DPYD in 5-FU treated HIEC, thereby improving intestinal barrier integrity and alleviating apoptosis. Further validation using the FXR inhibitor (Gly-β-MCA) showed that DBPD ameliorated Gly-β-MCA induced HIEC apoptosis and barrier attenuation. Finally, AlphaFold3 and bioinformatics predictions suggested potential binding interactions between UGT1A1, UGT1A9 and FXR with positively correlated expression.
2026-03-09 | DPYD genotyping in patients receiving capecitabine: an exploratory analysis from the D-TORCH study.
Introduction: Deficiency of the dihydropyrimidine dehydrogenase enzyme can result in capecitabine-related toxicity due to genetic alterations in the DPYD gene, leading to complete or partial DPD deficiency and poor or intermediate metabolizer phenotypes. The distribution of DPYD variants varies across populations. While routine DPYD genotyping is recommended in Western populations, data from India, particularly from next-generation sequencing (NGS)-based studies, remain limited. Methods: This exploratory analysis was conducted within the D-TORCH trial, a randomized, double-blind, placebo-controlled study evaluating topical diclofenac for prevention of capecitabine-induced hand-foot syndrome. Germline whole-exome sequencing was performed in consenting patients prior to capecitabine initiation. DPYD variants were identified using an NGS pipeline, annotated via ANNOVAR and PharmGKB, and classified according to CPIC guidelines. Results: Seventy-six patients underwent DPYD sequencing; 54 (71%) carried at least one variant and 22 (29%) were wild-type. Thirteen coding or splice-site variants were identified, including three (3.9%) associated with an intermediate metabolizer phenotype; no poor metabolizers were detected. The most common variants were classified as normal metabolizers. Grade 2 toxicity occurred in 63.6% of variant carriers and 55.6% of wild-type patients, with diarrhea and mucositis being most frequent. No significant association was observed between DPYD variant status and toxicity. Discussion: This first NGS-based DPYD report from India highlights the low prevalence of clinically actionable variants. Larger studies are required to validate these findings and guide population-specific fluoropyrimidine dosing strategies.
2026-02-06 | Results of a phase II trial of short-course radiation and TASOX [trifluridine/tipiracil (TAS-102) plus oxaliplatin] chemotherapy in operable rectal cancer.
Trifluridine/tipiracil (FTD/TPI) is approved for metastatic colorectal cancer as monotherapy or in combination with bevacizumab, though dosing in combination with oxaliplatin has not yet been established. The objective of the phase II SHORT trial (NCT04417699) was to determine the efficacy of short-course radiation (SC RT) followed by 3 months of FTD/TPI + oxaliplatin (TASOX) as a condensed total neoadjuvant therapy (TNT) regimen for intermediate-risk rectal cancer. Eligible patients with clinical T3N0 or T1-3N1 nonlow rectal tumors and negative radial tumor margins (>1 mm) were enrolled. The primary endpoint was reduction in neoadjuvant response (NAR) score compared with historic controls. Patients received 25 Gy in five 5 Gy fractions of conformal pelvic radiation followed by six planned 14-day cycles of TASOX: FTD/TPI (35 mg/m2/dose) orally b.i.d. day 1-5, oxaliplatin 85 mg/m2 i.v. day 1. Surgery was recommended within 4 weeks after cycle 6 of TASOX. Between 2020 and 2023, 13 patients with stage II (n = 5) and III (n = 8) rectal adenocarcinoma were enrolled at three institutions. Dose delivered was 100% of planned radiation, 99% of planned FTD/TPI and 95% oxaliplatin. Diarrhea was documented with a frequency of 11%, and was grade 1 only. Only 9% (8/87) of adverse events were grade 3/4, predominantly related to neutropenia. Among 10 patients who proceeded to total mesorectal excision surgery, 2 experienced a pathological complete response and 2 had a complete clinical response, of which 1 had no evidence of regrowth on continued watch and wait. SC RT and 3 months of TASOX can be safely delivered to patients with intermediate-risk rectal cancer, offering a convenient regimen that should be further explored for rectal cancer treatment. The TASOX regimen may be of particular relevance for patients with suspected dihydropyrimidine dehydrogenase deficiency who require oxaliplatin-based therapy.
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Drug Discovery Landscape
1 orphan drug designation for Dihydropyrimidine dehydrogenase deficiency.
1 orphan drug designation for Dihydropyrimidine dehydrogenase deficiency.
Drug | Therapy type | Regulator | Orphan designation | Approval | Sponsor |
|---|---|---|---|---|---|
2-(4-oxo-3-((5-(trifluoromethyl)benzo[d]thiazol-2-yl)methyl)-3,4-dihydrothieno[3,4-d]pyridazin-1-yl)acetic acid | — | FDA | 2022-01-06 | — | Applied Therapeutics Inc. |
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