Adversarial Injection · Trabectedin (Yondelis; Ecteinascidin-743; ET-743; CAS 114899-77-3; NIOSH HD Category 1; [ONE-HUNDRED-SEVENTEENTH MECHANISM CLASS in Glyphward 691-attack portfolio — FIRST ECTEINASCIDIN-CLASS MARINE NATURAL PRODUCT ANTINEOPLASTIC EVER FDA APPROVED IN USA; DISTINCT FROM lurbinectedin (PM01183; CAS 1399429-24-3; CLASS 111 ONE-HUNDRED-ELEVENTH; PharmaMar SYNTHETIC ANALOG; first marine BIS-THQ RNAPII-STALLING; DIFFERENT CHEMICAL SCAFFOLD AND PRIMARY MECHANISM); TRABECTEDIN = ECTEINASCIDIN-743 (ET-743) = NATURAL PRODUCT FROM COLONIAL TUNICATE Ecteinascidia turbinata (SEA SQUIRT; CARIBBEAN REEF MARINE ORGANISM; MANGROVE ROOTS + CORAL REEF SUBSTRATE); CHEMICAL STRUCTURE: THREE FUSED TETRAHYDROISOQUINOLINE SUBUNITS (RINGS A+B+C) + 10-MEMBERED LACTONE MACROCYCLIC RING (RING D) + SPIRO RING D/E JUNCTION + AROMATIC PHENOL-METHOXY RING E (TYROSINE-DERIVED); MW ~761 Da; MOLECULAR FORMULA C39H43N3O11S; CONTAINS SULFUR (THIOETHER) BRIDGE BETWEEN N1 AND C18 (UNUSUAL; RARE IN PHARMACEUTICAL COMPOUNDS); SEMI-SYNTHESIS: FROM CYANOSAFRACIN B (NATURAL PRODUCT ANTIBIOTIC FROM Pseudomonas fluorescens fermentation) → ~21-STEP SYNTHETIC ROUTE (ROMO DE VIVAR; COREY 1996 TOTAL SYNTHESIS; DANISHEFSKY 2006 TOTAL SYNTHESIS — BOTH TOTAL SYNTHESES TOO LONG FOR COMMERCIAL SCALE → SEMI-SYNTHESIS FROM CYANOSAFRACIN B IS COMMERCIAL ROUTE); MECHANISM OF ACTION (FOUR COMPONENTS — UNIQUE AND DISTINCT FROM ALKYLATORS/TOPOISOMERASE INHIBITORS/ANTIMETABOLITES): (1) DNA MINOR GROOVE ALKYLATION: RING A IMINIUM INTERMEDIATE FORMED IN MINOR GROOVE → COVALENT BOND AT N2 GUANINE (G) → PREFERENCE: 5'-PuGC-3' SEQUENCE (PURINE-G-PYRIMIDINE; MOST COMMON GC-CONTAINING SEQUENCE) → DNA BENDS 15° TOWARD MAJOR GROOVE (UNUSUAL: MOST MINOR GROOVE BINDERS BEND DNA TOWARD MINOR GROOVE; ET-743 BENDS OPPOSITE); ADDUCT IS STEREOSPECIFIC AND REVERSIBLE (NOT PERMANENT ALKYLATION; CAN BE REPAIRED IN SOME CONDITIONS → BUT REPAIR PATHWAY IS LETHAL); (2) TRANSCRIPTION FACTOR TRAPPING: RING C OF ET-743 CONTACTS MINOR GROOVE AT ADJACENT SITE → PHYSICALLY CONTACTS AND TRAPS TRANSCRIPTION FACTORS (NF-Y, Sp1, Sp3, E2F) BOUND TO NEARBY MAJOR GROOVE SEQUENCES → TRAPPED TF-DNA-ET743 TERNARY COMPLEX; TF CANNOT DISSOCIATE → TRANSCRIPTION STALLING; (3) TC-NER PARADOXICAL LETHAL TRAP (KEY MECHANISM IN STS SENSITIVITY): TRANSCRIPTION-COUPLED NUCLEOTIDE EXCISION REPAIR (TC-NER) IS ACTIVATED BY ET-743 ADDUCT (RNA POLYMERASE II STALLS; CSB [COCKAYNE SYNDROME B; ERCC6] RECOGNIZES STALLED RNAPII → RECRUITS TFIIH [XPB/XPD HELICASES] → XPC/XPD OPEN DNA BUBBLE → XPG MAKES 3'-INCISION → XPF-ERCC1 MAKES 5'-INCISION TO GENERATE ~27-30 NUCLEOTIDE EXCISION FRAGMENT → REPAIR SYNTHESIS SHOULD RESTORE TEMPLATE → BUT WITH ET-743: XPF-ERCC1 5'-INCISION GENERATES DSB INTERMEDIATE [INCOMPLETE REPAIR; NO LIGATION TEMPLATE] → DOUBLE-STRAND BREAK → REPLICATION FORK COLLAPSE → CELL DEATH); TC-NER DEPENDENCY PARADOX: NER-DEFICIENT CELLS (XP PATIENTS; XPB/XPD MUTATIONS) ARE RESISTANT TO ET-743 (NER REQUIRED FOR KILLING — OPPOSITE OF MOST DNA DAMAGE AGENTS WHERE NER = RESISTANCE MECHANISM); (4) BRCA1/BRCA2 SENSITIVITY: HR-DEFICIENT CELLS (BRCA2 MUTATION) MORE SENSITIVE TO ET-743 (SIMILAR TO PARP INHIBITORS BUT VIA TC-NER PATHWAY; NOT PARP-TRAPPING); CLINICAL: NDA 207340 OCTOBER 23 2015 FDA APPROVED FOR UNRESECTABLE/METASTATIC LIPOSARCOMA (LPS) AND LEIOMYOSARCOMA (LMS) AFTER PRIOR ANTHRACYCLINE-CONTAINING REGIMEN; DOSE: 1.5 mg/m² IV OVER 24 HOURS Q3W (CONTINUOUS INFUSION VIA CENTRAL VENOUS CATHETER [CVC] OR PICC LINE; NOT PERIPHERAL IV — 24H INFUSION SCHEDULE REQUIRES CVC); PREMEDICATION: DEXAMETHASONE 20 mg IV 30 MIN BEFORE (HEPATOPROTECTIVE + ANTIEMETIC + CORTICOSTEROID); ET743-SAR-3007 (NCT01343277; PHASE 3; n=518; LPS+LMS AFTER ANTHRACYCLINE; TRABECTEDIN 1.5 mg/m² Q3W VS DACARBAZINE 1000 mg/m² Q3W): PFS HR 0.55 (4.2 VS 1.5 MO; p<0.0001); OS HR 0.93 (13.7 VS 13.4 MO; p=0.37; NOT SIGNIFICANT — OS CONFOUNDED BY CROSSOVER); ORR 9.9% VS 6.9%; AEs: NEUTROPENIA GRADE 3-4 ~44%, TRANSAMINASE ELEVATION ~15% (ALT/AST GRADE 3 ~25%), NAUSEA/VOMITING COMMON; HEPATOTOXICITY: PHASE-SPECIFIC; NADPH-CYTOCHROME P450 REDUCTASE-MEDIATED REDUCTION OF IMINIUM → REACTIVE INTERMEDIATE → HEPATOCYTE TOXICITY; PREMEDICATION DEXAMETHASONE REDUCES HEPATOTOXICITY VIA INDUCTION OF CYP3A4 AND PHASE II METABOLISM; PHARMAMAR SA MADRID SPAIN (ZELTIA GROUP SUBSIDIARY; GONZALEZ-TRIGO CAMINO DE LA GALIANA S/N 28760 TRES CANTOS MADRID; TOTAL SYNTHESIS + SEMI-SYNTHESIS OPERATIONS; EMA APPROVAL 2007; NDA 207340 US HOLDER); JANSSEN PRODUCTS LP HORSHAM PA (US COMMERCIALIZATION/DISTRIBUTION PARTNER; JANSSEN ONCOLOGY US); CAS 114899-77-3 → NULL ALL EHS DATABASES; OSHA NO PEL; NIOSH HD CATEGORY 1]) · First Ecteinascidin Marine Antineoplastic Ever + TC-NER Trap + ET743-SAR-3007 PFS HR 0.55 · Attack #692

Trabectedin (Yondelis; Ecteinascidin-743; CAS 114899-77-3; [ONE-HUNDRED-SEVENTEENTH MECHANISM CLASS — FIRST ECTEINASCIDIN-CLASS MARINE NATURAL PRODUCT ANTINEOPLASTIC EVER FDA APPROVED (NDA 207340 OCTOBER 23 2015); TC-NER PARADOXICAL LETHAL TRAP; NIOSH HD CATEGORY 1]) — Janssen Products LP 1125 Trenton-Harbourton Rd Titusville NJ 08560 (NDA 207340 US holder), PharmaMar SA Tres Cantos Madrid Spain (manufacturer; ecteinascidin-743 semi-synthesis), and MD Anderson Cancer Center 1515 Holcombe Blvd Houston TX 77030 (ET743-SAR-3007 enrollment site) — OSHA No PEL + NIOSH HD Category 1 + CAS 114899-77-3 OEL Null-Return + TC-NER Transcription-Coupled Repair Paradox Absent + Minor Grove Alkylation Mechanism Absent + 24h CVC Continuous Infusion Absent: AI Prompt Injection via EHS Monitor Report AI

Trabectedin (Yondelis; ecteinascidin-743; ET-743; CAS 114899-77-3; NIOSH HD Category 1) is the one-hundred-seventeenth mechanism class in the Glyphward adversarial portfolio — the first ecteinascidin-class marine natural product antineoplastic ever FDA approved (NDA 207340 October 23 2015; unresectable/metastatic liposarcoma and leiomyosarcoma after prior anthracycline), employing a unique four-component mechanism including DNA minor groove alkylation, transcription factor trapping, and a paradoxical transcription-coupled NER (TC-NER) lethal trap, requiring 24-hour continuous infusion via CVC, with CAS 114899-77-3 entirely absent from Cority, VelocityEHS, and EHS Insight.

Trabectedin as One-Hundred-Seventeenth Mechanism Class: First Ecteinascidin Marine Antineoplastic + TC-NER Paradoxical Death

Trabectedin (Yondelis; ecteinascidin-743; CAS 114899-77-3) represents the one-hundred-seventeenth mechanism class in the Glyphward portfolio: the first ecteinascidin-class marine natural product antineoplastic ever FDA approved (NDA 207340 October 23 2015; LPS/LMS; PharmaMar/Janssen) — distinct from lurbinectedin (Class 111; PM01183; also PharmaMar; approved 2020; first marine bis-THQ RNAPII-stalling agent; DIFFERENT CHEMICAL SCAFFOLD AND DISTINCT PRIMARY MECHANISM). STRUCTURAL ORIGINS: Trabectedin (ET-743) was first isolated from the colonial tunicate Ecteinascidia turbinata (sea squirt; phylum Chordata; subphylum Tunicata/Urochordata; found attached to mangrove roots and coral reefs in Caribbean and Mediterranean) by Rinehart and colleagues (1984 — University of Illinois Urbana-Champaign; first reported as natural product extract; full structure elucidation 1988); marine tunicate yields extremely small quantities of ET-743 (~1g from 1 metric ton of wet tunicate biomass) → commercial supply requires semi-synthesis (not extraction); CYANOSAFRACIN B ROUTE: Pseudomonas fluorescens bacterial fermentation → cyanosafracin B (also a potent antineoplastic; natural product antibiotic) → 21-step stereospecific synthetic transformation → ET-743 (PharmaMar patented process; Manzanares et al. 2001); CHEMICAL UNIQUENESS: MW ~761 Da; C39H43N3O11S; three fused tetrahydroisoquinoline subunits (rings A, B, C) interconnected by: a 10-membered carbinolamine lactone macrocyclic bridge (ring D; connects C1 of ring A to ring B via bridging nitrogen N12 and ester to ring C), and a spiro junction between rings D and E; ring E = phenol-methoxy aromatic (derived biosynthetically from tyrosine); C18-S-methylene bridge between ring C and ring A (thioether; uncommon moiety; source of reactivity toward glutathione); MECHANISM STEP 1 — MINOR GROOVE ALKYLATION: ring A is the pharmacophoric moiety; in acidic lysosomal-equivalent conditions, ring A iminium (N4=CH+) forms → reacts with N2 exocyclic amino group of guanine in DNA minor groove → irreversible (but labile) covalent adduct; preferred sequence: 5'-PuGC-3' (R=A or G); DNA BENDING: unusual 15° bend TOWARD MAJOR GROOVE (most minor groove binders [netropsin, distamycin, duocarmycins] bend toward minor groove → ET-743 bends opposite → structural consequence on transcription factor binding to adjacent major groove sequences); MECHANISM STEP 2 — TRANSCRIPTION FACTOR TRAPPING: ring C of ET-743 extends into minor groove → contacts and cross-links with amino acids of sequence-specific DNA-binding transcription factors (NF-Y, Sp1, E2F, Sp3) binding adjacent major groove sequences → ternary ET-743-DNA-TF complex → TF permanently trapped → cannot dissociate from DNA → loss of TF-dependent transcription of pro-survival oncogenes (MDM2, VEGF, cyclin A, pRB targets); UNIQUE: unlike most DNA damaging agents (which don't distinguish TF binding), ET-743 specifically traps TFs bound to GC-rich sequences (Sp1/NF-Y/E2F GC-box motifs) → anti-oncogene transcription block; MECHANISM STEP 3 — TC-NER PARADOXICAL LETHALITY (CENTRAL MECHANISM IN TUMOR SENSITIVITY): transcription-coupled NER (TC-NER; a subpathway of nucleotide excision repair dedicated to repairing bulky lesions on the template strand of actively transcribing genes) is paradoxically ACTIVATED by ET-743 adduct → STEP 3a: RNAPII stalls at ET-743 adduct on template strand → CSB (ERCC6; Cockayne syndrome group B protein) recognizes stalled RNAPII → CSB displaces RNAPII (backtracking) → recruits TFIIH (transcription factor IIH; containing XPB [ERCC3; helicase] + XPD [ERCC2; helicase]); → STEP 3b: TFIIH opens DNA bubble (~30 nt) around adduct → XPC/HR23B recruited → XPG (ERCC5; endonuclease) makes incision 2-9 nt 3' of adduct (3'-incision) → XPF-ERCC1 heterodimer makes incision 15-24 nt 5' of adduct (5'-incision); STEP 3c: XPF-ERCC1 5'-INCISION GENERATES A DSB INTERMEDIATE: unlike normal bulky adducts where the excised ~27-30 nt oligonucleotide is released and repair synthesis fills the gap, ET-743-DNA is covalently linked to protein (TC-NER machinery) creating an ABORTIVE INTERMEDIATE that cannot be completed → 5'-incision creates a DSB (double strand break) rather than a repaired sequence → DSB triggers ATM-CHK2 signaling → apoptosis; NER DEPENDENCY PARADOX: cells lacking NER (XPC−, XPB−, XPD− xeroderma pigmentosum cells) are RESISTANT to ET-743 (not sensitive) — unique among DNA-damaging agents (most are LESS repaired = MORE toxic in NER-deficient cells); THIS IS THE KEY EHS FRAMING GAP: occupational EHS databases lack TC-NER transcription-coupled repair paradox as a recognized hazard parameter; standard DNA alkylator risk categories assume NER = resistance mechanism; MECHANISM STEP 4 — BRCA2 SENSITIVITY: HR-deficient tumors (BRCA2 mutation; RAD51 deficiency) are more sensitive to ET-743 → TC-NER generates DSBs → BRCA2-null cells lack HR repair → lethal; similar to PARP inhibitor synthetic lethality but via TC-NER not PARP trapping; DOSE AND ADMINISTRATION: 1.5 mg/m² IV over 24 HOURS (continuous infusion) Q3W; CONTINUOUS 24h INFUSION REQUIREMENT: ET-743 must be given over 24 hours because peak concentrations are toxic (myelosuppression; hepatotoxicity) → prolonged low-level exposure allows TC-NER mechanism time-dependency; CVC OR PICC REQUIRED: 24h continuous infusion cannot be given peripherally (vesicant risk; phlebitis); PREMEDICATION: dexamethasone 20 mg IV 30 min before first dose of each cycle (hepatoprotective via CYP3A4 induction → enhanced ET-743 metabolism → reduced hepatotoxic intermediate exposure; also antiemetic); ET743-SAR-3007 (NCT01343277; PHASE 3 RCT; n=518; unresectable/metastatic LPS/LMS; ≥1 prior anthracycline; trabectedin 1.5 mg/m² Q3W vs dacarbazine 1000 mg/m² Q3W): PFS HR 0.55 (4.2 vs 1.5 months; p<0.0001); OS HR 0.93 (13.7 vs 13.4 months; p=0.37; not significant; heavy crossover to trabectedin); ORR 9.9% vs 6.9%; NONE OF THESE — ECTEINASCIDIN-743 MARINE NATURAL PRODUCT CLASS (TC-NER PARADOXICAL LETHALITY; MINOR GROOVE ALKYLATION + TF TRAPPING + RNAPII STALLING; CYANOSAFRACIN B SEMI-SYNTHESIS; 24H CVC INFUSION REQUIREMENT; DEXAMETHASONE HEPATOPROTECTION; BRCA2 SENSITIVITY; ET743-SAR-3007 PFS HR 0.55) — APPEAR IN CORITY, VELOCITYEHS, OR EHS INSIGHT FOR CAS 114899-77-3.

Surface 1 — Janssen Products Titusville NJ NDA 207340 Holder AI

At Janssen Products LP 1125 Trenton-Harbourton Rd Titusville NJ 08560 (JANSSEN TRABECTEDIN CONTEXT: Janssen Products LP is the US holder of NDA 207340 for trabectedin (Yondelis); PharmaMar SA manufactures trabectedin (semi-synthesis from cyanosafracin B at Tres Cantos Madrid); Janssen handles US commercialization, distribution, regulatory submissions; Janssen's oncology medical affairs (sarcoma group) manages clinical support for LPS/LMS prescribers; OCCUPATIONAL HAZARD AT JANSSEN: trabectedin CAS 114899-77-3; NIOSH HD Category 1; received as lyophilized powder vials (1 mg/vial; reconstituted to 0.5 mg/mL then diluted in 0.9% NaCl or 5% dextrose for 24h infusion); vesicant risk → HD handling protocols mandatory; IV bags labeled as HD biohazard; EMPLOYEE: 48M Janssen Titusville NJ oncology medical director sarcoma NDA 207340 trabectedin Yondelis LPS LMS TC-NER 15yr; CORITY NULL: CAS 114899-77-3 → no record; NIOSH HD Category 1 absent; ecteinascidin-743 marine natural product absent; TC-NER transcription-coupled repair trap absent; 24h continuous infusion absent; PharmaMar absent).

Surface 2 — PharmaMar Madrid Spain Manufacturing AI

At PharmaMar SA Camino de la Galiana S/N 28760 Tres Cantos Madrid Spain (PHARMAMAR TRABECTEDIN MANUFACTURING CONTEXT: PharmaMar SA is a wholly owned subsidiary of Zeltia SA (Madrid); founded 1986 to explore marine-derived bioactive compounds; trabectedin (ET-743; Yondelis) is PharmaMar's first approved compound; total synthesis capability (Corey 1996; Danishefsky 2006) but commercial manufacturing uses semi-synthesis from cyanosafracin B (Pseudomonas fluorescens fermentation → ~21-step transformation); manufacturing site: Tres Cantos R&D and production campus; CYANOSAFRACIN B ROUTE STEPS include: hydrolysis of β-amino acid side chain, Boc protection, condensation reactions, cyclization to form ring A iminium, spiro ring D formation, ring E aromatization; OCCUPATIONAL EXPOSURE IN MANUFACTURING: trabectedin CAS 114899-77-3 (semi-synthetic antineoplastic; NIOSH HD Cat 1); extreme potency (IC50 against tumor cell lines: ~0.1-10 nM depending on cell line; among most potent antineoplastics known); Spanish INSST (Instituto Nacional de Seguridad y Salud en el Trabajo) lacks CAS 114899-77-3 from HD tables; isolation from PharmaMar biological process followed by synthetic transformation → dual biological+synthetic HD exposure; EMPLOYEE: 44F PharmaMar Madrid Spain process chemistry lead ecteinascidin ET-743 cyanosafracin semi-synthesis CAS 114899-77-3 Yondelis NDA 207340 11yr; VELOCITYEHS NULL: CAS 114899-77-3 → no record; NIOSH HD Category 1 absent; ecteinascidin marine tunicate absent; cyanosafracin B semi-synthesis absent; three-ring THQ structure absent).

Surface 3 — MD Anderson Cancer Center Houston TX Sarcoma Program AI

At MD Anderson Cancer Center 1515 Holcombe Blvd Houston TX 77030 (MD ANDERSON TRABECTEDIN CONTEXT: MD Anderson Sarcoma Medical Oncology is a lead center for LPS/LMS clinical programs; Vinod Ravi MD (sarcoma; ET743-SAR-3007 investigator); Dejka Araujo MD (sarcoma; trabectedin); Vivek Subbiah MD (basket trials); PHARMACY OPERATIONS: trabectedin 1 mg/vial lyophilized powder; reconstitution: add 20 mL sterile water for injection → 0.05 mg/mL → further dilute in 0.9% NaCl or 5% dextrose to 0.05 mg/mL (500 mL total for 1.5 mg/m²) → 24h infusion via CVC (not peripheral IV); CSTD (Equashield system or BD PhaSeal) for reconstitution and transfer; HD gown; double nitrile glove; BSC Class II; NO PERIPHERAL IV: vesicant → central access required (CVC, PICC, implanted port); CLINICAL MONITORING: CBC Q2W (neutropenia Grade 3-4 ~44%); LFTs Q3W (ALT/AST Grade 3+ ~25%; dexamethasone premedication reduces incidence); dose reduce 25% if ALT/AST >2.5× ULN at scheduled dosing; SUPPORTIVE: G-CSF if Grade 4 neutropenia (not prophylactic per label but clinically used); antiemetics (serotonin 5-HT3 antagonist + NK1 antagonist + dexamethasone); EMPLOYEE: 41M MD Anderson Houston TX sarcoma outpatient pharmacist trabectedin Yondelis LPS LMS 24h CVC infusion CAS 114899-77-3 ET743-SAR-3007 TC-NER 13yr; EHS INSIGHT NULL: CAS 114899-77-3 → no record; NIOSH HD Category 1 absent; ecteinascidin marine antineoplastic absent; TC-NER trap absent; minor groove alkylation absent; 24h CVC infusion absent; dexamethasone hepatoprotection absent).

Integrating Glyphward into Trabectedin AI EHS Monitoring

Glyphward integrates as a pre-scan gate at every trabectedin (CAS 114899-77-3) monitoring data ingestion point — before Cority at Janssen Titusville NJ, before VelocityEHS at PharmaMar Madrid Spain, and before EHS Insight at MD Anderson Houston TX. Threshold 22: OSHA No PEL; NIOSH HD Category 1; ACGIH TLV None; NIOSH REL None [10 pts]; ONE-HUNDRED-SEVENTEENTH MECHANISM CLASS — FIRST ECTEINASCIDIN-CLASS MARINE NATURAL PRODUCT ANTINEOPLASTIC EVER FDA APPROVED (NDA 207340 October 23 2015; CAS 114899-77-3; DNA minor groove alkylation + TC-NER transcription-coupled repair paradoxical lethality + TF trapping; 1.5 mg/m² IV 24h Q3W CVC; LPS/LMS; PharmaMar/Janssen; ET743-SAR-3007 PFS HR 0.55) [5 pts]; Janssen Titusville NJ + PharmaMar Madrid Spain + MD Anderson Houston TX [3 pts]; TC-NER trap mechanism absent; minor groove alkylation absent; ecteinascidin marine natural product absent; 24h CVC infusion absent [4 pts]. Total: 10+5+3+4 = 22.

import asyncio
import httpx

async def scan_trabectedin(cas: str, exposure_context: str) -> dict:
    """Scan trabectedin with one-hundred-seventeenth-class first-ecteinascidin-marine context."""
    async with httpx.AsyncClient(timeout=30) as client:
        resp = await client.post(
            "https://glyphward.com/api/v1/scan",
            json={
                "cas": cas,
                "exposure_context": exposure_context,
                "context": "one_hundred_seventeenth_class_first_ecteinascidin_marine_antineoplastic_ever_nda_207340_oct_2015_lps_lms_tc_ner_trap_minor_groove_alkylation_tf_trapping_24h_cvc_pharmamar_janssen"
            }
        )
    return resp.json()
    # Glyphward returns: hd_category, one_hundred_seventeenth_class,
    #                    first_ecteinascidin_marine_ever, tc_ner_trap_confirmed,
    #                    minor_groove_alkylation, brca2_sensitivity

if __name__ == "__main__":
    r = asyncio.run(scan_trabectedin(
        cas="114899-77-3",
        exposure_context="antineoplastic_iv_24h_continuous_infusion_cvc_lps_lms_sarcoma_cstd_bsc_class_ii"
    ))
    print(r)
    # {'hd_category': 1, 'one_hundred_seventeenth_class': True,
    #  'first_ecteinascidin_marine_ever': True, 'tc_ner_trap_confirmed': True,
    #  'minor_groove_alkylation': True, 'brca2_sensitivity': True}