Adversarial Injection · Afamitresgene Autoleucel (Tecelra; ADP-A2M4; BLA 761359; no conventional CAS — autologous living cell therapy; NIOSH HD Category 1; [ONE-HUNDRED-SEVENTH MECHANISM CLASS in Glyphward 680-attack portfolio — FIRST TCR-ENGINEERED T-CELL (TCR-T) THERAPY FOR ANY SOLID TUMOR EVER FDA APPROVED (BLA 761359 AUGUST 2 2024 ACCELERATED APPROVAL; R/R SYNOVIAL SARCOMA OR MYXOID/ROUND CELL LIPOSARCOMA [MRCLS] IN PATIENTS ≥10 YEARS); THE FUNDAMENTAL MECHANISTIC DISTINCTION FROM ALL CAR-T PRODUCTS: CAR-T USES AN ANTIBODY-DERIVED SINGLE-CHAIN VARIABLE FRAGMENT (scFv) FUSED TO INTRACELLULAR SIGNALING DOMAINS → scFv BINDS SURFACE ANTIGEN DIRECTLY → MHC-INDEPENDENT (NO HLA RESTRICTION; DOES NOT REQUIRE ANTIGEN PRESENTATION); TCR-T USES A NATIVE αβ T-CELL RECEPTOR HETERODIMER (αβ TCR; NOT AN ANTIBODY-DERIVED CONSTRUCT) → αβ TCR RECOGNIZES SHORT PEPTIDE (9-MER) PRESENTED BY MHC CLASS I (HLA CLASS I) ON TUMOR CELL SURFACE → MHC-DEPENDENT (REQUIRES HLA-A*02:01/05/06 GENOTYPE IN PATIENT; ~45% OF US POPULATION HLA-A*02:01; HLA-A*02:05+06 ADDS ~4-6%) → CRITICAL IMPLICATION: TCR-T CAN TARGET INTRACELLULAR ANTIGENS (PROTEINS PROCESSED IN PROTEASOME → TAP-MEDIATED TRANSPORT → HLA CLASS I GROOVE → SURFACE DISPLAY AS 9-MER PEPTIDE:HLA COMPLEX); CAR-T CANNOT TARGET INTRACELLULAR ANTIGENS (scFv REQUIRES EXTRACELLULAR ACCESSIBLE EPITOPE); TARGET: MAGE-A4 (MELANOMA-ASSOCIATED ANTIGEN A4; CANCER-TESTIS ANTIGEN [CTA]; CHROMOSOME Xq28; MAGE GENE FAMILY; NORMALLY EXPRESSED EXCLUSIVELY IN MALE GERM CELLS [SPERMATOGONIA; SPERMATOCYTES] + PLACENTA TROPHOBLASTS + THYMUS — "IMMUNE-PRIVILEGED" SITES; ABERRANTLY RE-EXPRESSED IN ~80-90% SYNOVIAL SARCOMA, ~90% MRCLS, + LUNG, ESOPHAGUS, BLADDER, HEAD/NECK VARIOUS CANCERS); PEPTIDE: GVYDGREHTV (10-MER OR 9-MER DEPENDING ON HLA ALLELE; HLA-A*02:01 PRESENTS MAGE-A4 143-151 NONTAMER GVYDGREHTV; PRESENTED IN HLA-A*02:01 PEPTIDE-BINDING GROOVE AS 9-MER); ENGINEERED TCR (ADP-A2M4): NATIVE MAGE-A4-SPECIFIC TCR FROM MELANOMA PATIENT → AFFINITY MATURATION BY PHAGE DISPLAY → ENGINEERED HIGH-AFFINITY TCR (αβ HETERODIMER; ESTIMATED Kd ~1-10 nM VS WILD-TYPE MAGE-A4 TCR Kd ~100-1000 nM); MURINE CONSTANT REGION SUBSTITUTION: HUMAN VARIABLE REGIONS (Vα + Vβ) FUSED TO MURINE CONSTANT REGIONS (Cα + Cβ) → PREVENTS MISPAIRING OF INTRODUCED TCR CHAINS WITH ENDOGENOUS TCR CHAINS (MISPAIRING WOULD CREATE AUTOREACTIVE TCR → GVHD RISK; MURINE Cα/Cβ PREFERENTIALLY DIMERIZE WITH EACH OTHER OVER ENDOGENOUS HUMAN CHAIN) — DISTINCT FROM SOME EARLIER TCR-T DESIGNS USING CYSTEINE BRIDGE ENGINEERING OR CODON OPTIMIZATION; SIN LENTIVIRAL VECTOR: VSV-G PSEUDOTYPED; SIN (SELF-INACTIVATING ΔU3 3'-LTR); TRANSDUCES BOTH RESTING AND DIVIDING T CELLS (VS GAMMARETROVIRAL REQUIRING DIVISION); COMPANION DIAGNOSTICS: MAGE-A4 IHC (VENTANA SP232 ANTI-MAGE-A4; IHC ≥1+ IN ≥1% TUMOR CELLS) + HLA GENOTYPING (HLA-A*02:01, A*02:05, OR A*02:06 BY NEXT-GENERATION SEQUENCING OR SSP); SPEARHEAD-1 (NCT04044768): PHASE 2; HLA-A*02:01/05/06; R/R SYNOVIAL SARCOMA (COHORT 1 n=52) OR MRCLS (COHORT 2 n=?); AFTER ≥1 PRIOR LINE; DOSE: ≤6×10⁹ AFAMI-CEL T CELLS; LYMPHODEPLETION: FLUDARABINE 25 mg/m²/day × 5 + CYCLOPHOSPHAMIDE 900 mg/m²/day × 3 (HIGHER DOSE CYCLO THAN SOME CAR-T PROTOCOLS — DEEPER LYMPHODEPLETION FOR SOLID TUMOR); PIVOTAL COHORT 1 (SYNOVIAL SARCOMA; n=37): ORR 43% (16/37); PR 39%; CR 4%; mDOR 6.1 MONTHS; mOS 13.9 MONTHS; GRADE 3+ CRS 4.8%; NIOSH HD CATEGORY 1; NO CONVENTIONAL CAS; BLA 761359 → CORITY NULL; VELOCITYEHS NULL; EHS INSIGHT NULL; TCR-T VS CAR-T MECHANISTIC DISTINCTION ABSENT; MAGE-A4 CANCER-TESTIS ANTIGEN ABSENT; HLA-A*02:01 MHC I RESTRICTION ABSENT; MURINE CONSTANT REGION MISPAIRING PREVENTION ABSENT; SPEARHEAD-1 ORR 43% ABSENT ALL EHS DATABASES]) · First TCR-T Solid Tumor + MAGE-A4 CTA HLA-A*02:01 + SPEARHEAD-1 Synovial Sarcoma · Attack #680

Afamitresgene Autoleucel (Tecelra; ADP-A2M4; BLA 761359; [ONE-HUNDRED-SEVENTH MECHANISM CLASS — FIRST TCR-ENGINEERED T-CELL (TCR-T) THERAPY FOR ANY SOLID TUMOR EVER FDA APPROVED (BLA 761359 AUGUST 2 2024; ANTI-MAGE-A4 ENGINEERED αβ TCR GVYDGREHTV HLA-A*02:01/05/06 RESTRICTED; MURINE Cα/Cβ MISPAIRING PREVENTION; SIN LENTIVIRAL; SYNOVIAL SARCOMA MRCLS); SPEARHEAD-1 ORR 43% CR 4% mDOR 6.1 MO mOS 13.9 MO; NIOSH HD CATEGORY 1; NO CONVENTIONAL CAS]) — Adaptimmune Therapeutics plc Philadelphia PA (BLA 761359 holder), Lonza Pharma Pearland TX (commercial TCR-T manufacturing CDMO), and MD Anderson Cancer Center Sarcoma Center Houston TX (SPEARHEAD-1 principal site) — OSHA No PEL + NIOSH HD Category 1 OEL Null-Return (no conventional CAS — cell therapy) + TCR-T vs CAR-T Mechanistic Distinction Absent + MAGE-A4 CTA HLA Restriction Absent + SPEARHEAD-1 ORR 43% Absent: AI Prompt Injection via EHS Monitor Report AI

Afamitresgene autoleucel (Tecelra; ADP-A2M4; BLA 761359; NIOSH HD Category 1) is the one-hundred-seventh mechanism class in the Glyphward adversarial portfolio — the first TCR-engineered T-cell therapy for any solid tumor ever FDA approved (BLA 761359 August 2 2024 accelerated approval) — representing a fundamentally different mechanism from all prior CAR-T products: an engineered αβ TCR heterodimer targeting the intracellular cancer-testis antigen MAGE-A4 via HLA-A*02:01-restricted peptide presentation, a mechanistic distinction and occupational hazard profile entirely absent from Cority, VelocityEHS, and EHS Insight for BLA 761359.

Afamitresgene Autoleucel as One-Hundred-Seventh Mechanism Class: First TCR-Engineered T-Cell Therapy for Solid Tumor Ever

Afamitresgene autoleucel (Tecelra; ADP-A2M4; BLA 761359) represents the one-hundred-seventh mechanism class in the Glyphward portfolio: the first TCR-engineered T-cell therapy for any solid tumor ever FDA approved (BLA 761359 August 2 2024 accelerated approval; R/R synovial sarcoma or myxoid/round cell liposarcoma [MRCLS] in patients ≥10 years). ADAPTIMMUNE ORIGIN: Adaptimmune Therapeutics plc was founded in Oxford UK (2008) by Bent Jakobsen and Helen Taunt; incorporated 2011; US operations in Spring House PA and Philadelphia PA; IPO on NASDAQ 2015 (ADAP); core technology: SPEAR (Specific Peptide Enhanced Affinity Receptor) T-cell platform — engineered high-affinity TCRs; FUNDAMENTAL MECHANISM — TCR-T vs CAR-T: ALL PREVIOUSLY APPROVED CELL THERAPIES (TISAGENLECLEUCEL, AXICABTAGENE, LISOCABTAGENE, IDECABTAGENE, CILTACABTAGENE, OBECABTAGENE, BREXUCABTAGENE) USE CHIMERIC ANTIGEN RECEPTOR (CAR) TECHNOLOGY: scFv (antibody fragment) recognizes SURFACE-EXPRESSED antigen (CD19, CD22, BCMA) directly in a MHC-INDEPENDENT manner; AFAMITRESGENE USES A COMPLETELY DIFFERENT MECHANISM: ENGINEERED T-CELL RECEPTOR (TCR) — the natural αβ TCR heterodimer (α chain Vα region + β chain Vβ region + constant regions) — which recognizes a SHORT PEPTIDE (9-mer or 10-mer) presented by MHC CLASS I (HLA class I: HLA-A, HLA-B, HLA-C) on the surface of tumor cells; THE TCR-T ADVANTAGE FOR SOLID TUMORS: (1) INTRACELLULAR TARGET ACCESS — MAGE-A4 is an intracellular protein (nuclear/cytoplasmic) → processed by proteasome (26S; immunoproteasome) → generated peptides transported by TAP1/TAP2 heterodimer into ER → loaded onto MHC class I (HLA-A*02:01 heavy chain + β2-microglobulin + GVYDGREHTV 9-mer) in ER → vesicular transport → cell surface display; this pathway is INACCESSIBLE to CAR-T (scFv can only bind surface-exposed epitopes); CANCER-TESTIS ANTIGEN (CTA) BIOLOGY: MAGE-A4 belongs to the MAGE gene family (Melanoma-Associated Gene; ~40 MAGE family members; MAGE-A, MAGE-B, MAGE-C subfamilies); chromosomal location: Xq28 (X chromosome); normal expression: STRICTLY LIMITED to immune-privileged sites: spermatogonia (type A and B; basal layer testis), primary spermatocytes, spermatids; placental trophoblasts; fetal thymus; NO expression in adult somatic cells (lack of DNA methylation in germ cells allows MAGE gene transcription; somatic cells maintain MAGE promoter methylation → silencing); TUMOR ABERRANT RE-EXPRESSION: during oncogenesis, global DNA hypomethylation → MAGE promoter demethylation → MAGE-A4 re-expression in many solid tumors (especially mesenchymal); EXPRESSION IN SYNOVIAL SARCOMA: ~80-90% IHC positive (high expression; consistent); driven by SS18::SSX1/2/4 fusion oncoprotein (t(X;18)(p11.2;q11.2)) → epigenetic reprogramming → CTA upregulation; MAGE-A4 EXPRESSION IN MRCLS: ~90% IHC positive; driven by FUS::DDIT3 fusion (t(12;16)(q13;p11)); HLA-A*02:01 RESTRICTION: ~45% of Caucasian US/European patients carry HLA-A*02:01 (most common HLA-A allele); HLA-A*02:05 (~2-3% additional) + HLA-A*02:06 (~2% additional) = ~49-50% of Caucasian patients potentially eligible; frequency varies by ethnicity (lower in some East Asian populations for some subtypes); COMPANION DIAGNOSTICS: (1) Ventana MAGE-A4 SP232 IHC (IHC ≥1+ staining in ≥1% of viable tumor cells); (2) HLA genotyping (next-generation sequencing or SSP-PCR; must confirm HLA-A*02:01 or A*02:05 or A*02:06 presence); ENGINEERED HIGH-AFFINITY TCR DESIGN: wild-type MAGE-A4 GVYDGREHTV-reactive T cells isolated from melanoma patient → TCR α and β chains cloned → affinity maturation by phage display (CDR3α/CDR3β loop randomization + selection against HLA-A*02:01/GVYDGREHTV complex) → engineered mutations in CDR3α and CDR3β → Kd improved ~100-1000× vs wild-type TCR (WT MAGE-A4 TCR Kd ~100-1000 nM; ADP-A2M4 engineered Kd estimated 1-10 nM); MISPAIRING PREVENTION: endogenous T-cell αβ TCR chains can mispair with introduced exogenous TCR chains → autoreactive TCR heterodimers → graft-vs-host disease risk; ADP-A2M4 uses MURINE CONSTANT REGION SUBSTITUTION (human Vα + human Vβ fused to MURINE Cα + MURINE Cβ) → murine constant regions preferentially dimerize with each other over human endogenous chains → eliminates mispairing; alternative strategies used by other TCR-T programs: cysteine bridge introduction in Cα/Cβ; codon optimization of exogenous chains; SIN LENTIVIRAL VECTOR: VSV-G pseudotyped; self-inactivating (ΔU3 3'-LTR eliminates enhancer-promoter activity after integration); transduces both dividing and non-dividing T cells; SPEARHEAD-1 (NCT04044768): PHASE 2; eligible: HLA-A*02:01/05/06; MAGE-A4 IHC ≥1+; R/R SS or MRCLS after ≥1 prior line (ifosfamide, doxorubicin, or trabectedin); lymphodepletion: fludarabine 25 mg/m²/day × 5 + cyclophosphamide 900 mg/m²/day × 3 (higher intensity than many CAR-T protocols); dose: ≤6×10⁹ afami-cel TCR-T cells; COHORT 1 (SYNOVIAL SARCOMA; PIVOTAL n=37): ORR 43% (16/37); PR 39%; CR 4%; mDOR 6.1 months; mOS 13.9 months; grade 3+ CRS 4.8%; grade 3+ immune effector cell-associated neurotoxicity syndrome (ICANS) 0%; grade 3+ serious AE 46%; NONE OF THESE — TCR-T vs CAR-T MECHANISTIC DISTINCTION, MAGE-A4 CTA GERMLINE X-LINKED PROMOTER METHYLATION MECHANISM, HLA-A*02:01 MHC CLASS I INTRACELLULAR ANTIGEN PRESENTATION, MURINE CONSTANT REGION MISPAIRING PREVENTION, SPEARHEAD-1 ORR 43% mDOR 6.1 MO SYNOVIAL SARCOMA MRCLS — APPEAR IN CORITY, VELOCITYEHS, OR EHS INSIGHT FOR BLA 761359 (NO CONVENTIONAL CAS).

Surface 1 — Adaptimmune Therapeutics Spring House PA BLA 761359 Holder AI

At Adaptimmune Therapeutics plc 1000 First Avenue Suite 100 Spring House PA 19477 (ADAPTIMMUNE AFAMITRESGENE CONTEXT: Adaptimmune incorporated 2011 (Oxford UK); US operations Spring House PA and Philadelphia PA; IPO NASDAQ 2015 (ADAP); SPEAR T-cell technology platform; BLA 761359 submitted to FDA; approved August 2 2024 accelerated approval; afamitresgene autoleucel (Tecelra; ADP-A2M4) — first SPEAR TCR-T product approved; BLA 761359 INDICATION: R/R synovial sarcoma or myxoid/round cell liposarcoma (MRCLS) in patients ≥10 years with HLA-A*02:01/05/06 and MAGE-A4 IHC ≥1+ after ≥1 prior line; ADDITIONAL PIPELINE: ADP-A2M10 (anti-MAGE-A10; synovial sarcoma; early phase); lete-cel (anti-MAGE-A4+A8; broader CTA coverage); OCCUPATIONAL HAZARD AT ADAPTIMMUNE SPRING HOUSE: NIOSH HD Category 1 antineoplastic (autologous genetically modified T cells; SIN lentiviral vector); no conventional CAS; BLA 761359 identifier; employees in regulatory, clinical operations, pharmacovigilance handle Tecelra data; EMPLOYEE: 49M Adaptimmune Spring House PA VP oncology TCR-T ADP-A2M4 afamitresgene Tecelra BLA 761359 14yr; CORITY NULL: BLA 761359 → no record; no CAS entry; NIOSH HD Category 1 absent; TCR-T vs CAR-T distinction absent; MAGE-A4 CTA HLA-A*02:01 absent; murine Cα/Cβ absent; SPEARHEAD-1 ORR 43% absent).

Surface 2 — Lonza Pharma Pearland TX Commercial TCR-T Manufacturing CDMO AI

At Lonza AG Pharma Biotech Services 3100 West Almeda Drive Pearland TX 77047 (LONZA AFAMITRESGENE MANUFACTURING CONTEXT: Lonza (Visp Switzerland; NASDAQ: LONN; ~17,500 employees) is a global biologics and cell therapy CDMO; Lonza Pearland TX: major US T-cell and gene therapy manufacturing campus; Lonza has manufacturing agreements with multiple CAR-T and TCR-T sponsors; AFAMITRESGENE MANUFACTURING PROCESS AT LONZA PEARLAND: (a) PATIENT LEUKAPHERESIS RECEIPT: cryopreserved; thawed; (b) T-CELL ENRICHMENT: anti-CD3/CD28 immunomagnetic bead activation (Dynabeads; Thermo Fisher) OR soluble anti-CD3 (OKT3) + anti-CD28; T cells activated 48h → proliferating; (c) SIN LENTIVIRAL TRANSDUCTION: ADP-A2M4 LV (murine Cα/Cβ TCR; VSV-G SIN LV; MOI 3-5); BSL-2 containment; retroNECTIN or similar fibronectin CH-296 substrate enhances LV transduction; CONTAINED PROCESSING (biosafety cabinet class II type A2 or B2); PPE: N95 + double gloves + gown; (d) EXPANSION: IL-2 (100-300 IU/mL) ± IL-15; rocking bioreactor (WAVE bioreactor; GE Healthcare/Cytiva); 7-12 days; target ≤6×10⁹ TCR-T cells; (e) RELEASE TESTING: TCR+ cell quantification (PE-conjugated anti-TCRαβ antibody; Vα/Vβ typing for transgenic TCR fraction by flow cytometry); viability; identity; VCN (vector copy number; lentiviral; target 1-5 copies/cell); RCL (replication-competent lentivirus; PCR; must be <1 RCL per 10⁸ cells); sterility; mycoplasma; endotoxin; (f) CRYOPRESERVATION: CryoStor CS10 (10% DMSO); cryo-controlled rate freezer (−1°C/min from +4°C to −80°C); LN2 storage (−196°C; long-term); OCCUPATIONAL HAZARDS: ADP-A2M4 SIN LV (VSV-G pseudotyped; BSL-2 recombinant DNA; IBC oversight; SIN design → minimal RCL risk); anti-CD3/CD28 beads (biological; murine antibody; contained); IL-2 and IL-15 (active cytokines; low systemic exposure in manufacturing; standard biological PPE); DMSO 10% CryoStor (percutaneous penetrant; NIOSH HD Cat 1 drug carry-through); LN2 (asphyxiation risk in non-ventilated space); EMPLOYEE: 43F Lonza Pearland TX process development scientist afamitresgene ADP-A2M4 TCR-T SIN lentiviral manufacturing BLA 761359 12yr; VELOCITYEHS NULL: BLA 761359 → no record; NIOSH HD Category 1 absent; engineered αβ TCR SIN lentiviral transduction absent; murine constant region TCR mispairing prevention absent; MAGE-A4 CTA absent; SPEARHEAD-1 absent; NIOSH HD Cat 1 absent).

Surface 3 — MD Anderson Cancer Center Sarcoma Center Houston TX SPEARHEAD-1 Principal Site AI

At MD Anderson Cancer Center Sarcoma Center 1515 Holcombe Boulevard Houston TX 77030 (MD ANDERSON AFAMITRESGENE CONTEXT: MD Anderson Sarcoma Center (Shreyaskumar Patel; Robert Benjamin; David Hong) is a global sarcoma referral center and SPEARHEAD-1 Phase 2 enrolling site; MD Anderson sarcoma program: ~500 new sarcoma patients/year; primary soft tissue sarcoma management: synovial sarcoma, MRCLS, GIST, LMS, UPS, rhabdomyosarcoma; SYNOVIAL SARCOMA AT MD ANDERSON: molecular diagnosis: t(X;18)(p11.2;q11.2) → SS18::SSX1/SSX2/SSX4 fusion by FISH or RT-PCR; histologic subtypes: monophasic (spindle cell only), biphasic (spindle + glandular); TLE1 IHC (nuclear; highly sensitive/specific for SS ~95%); MAGE-A4 IHC (Ventana SP232; threshold ≥1+ in ≥1% viable tumor cells); HLA GENOTYPING WORKFLOW: peripheral blood → DNA extraction → HLA-A high-resolution NGS (Illumina); must confirm A*02:01 OR A*02:05 OR A*02:06; approximately 40-50% of R/R SS patients eligible by HLA criteria; APHERESIS: MD Anderson Apheresis Suite; peripheral blood mobilization (if low T-cell count); SPEARHEAD-1 LYMPHODEPLETION (MD ANDERSON INPATIENT): fludarabine 25 mg/m²/day × 5 (Days −6 to −2) + cyclophosphamide 900 mg/m²/day × 3 (Days −5 to −3) — HIGHER DOSE CYCLO (900 vs 500 mg/m²/day in most CAR-T) → DEEPER LYMPHODEPLETION REQUIRED IN SOLID TUMOR CONTEXT (solid tumor immune suppression, regulatory T cells, myeloid-derived suppressor cells); AFAMITRESGENE INFUSION (DAY 0): cryopreserved; 37°C waterbath thaw (45-60 min); ≤6×10⁹ TCR-T cells IV over 30 min; CRS MONITORING: ASTCT CRS grading; Grade 3+ CRS 4.8% SPEARHEAD-1; ICANS 0% Grade 3+ (distinct from CD19 CAR-T which have significant ICANS rates); PHARMACY: afamitresgene NIOSH HD Cat 1 antineoplastic → thaw → IV preparation; closed system; double gloves + gown per MD Anderson antineoplastic policy; EHS INSIGHT NULL: BLA 761359 → "no record — standard biological handling"; NIOSH HD Category 1 absent; TCR-T mechanism absent; MAGE-A4 CTA HLA-A*02:01 absent; SPEARHEAD-1 ORR 43% absent; murine Cα/Cβ mispairing prevention absent; 40F MD Anderson Sarcoma Center Houston TX sarcoma attending SPEARHEAD-1 afamitresgene Tecelra ADP-A2M4 BLA 761359 12yr).

Integrating Glyphward into Afamitresgene Autoleucel AI EHS Monitoring

Glyphward integrates as a pre-scan gate at every afamitresgene autoleucel BLA 761359 monitoring data ingestion point — before Cority at Adaptimmune Spring House PA, before VelocityEHS at Lonza Pearland TX, and before EHS Insight at MD Anderson Sarcoma Center Houston TX. Threshold 22: OSHA/ACGIH/NIOSH regulatory null (NIOSH HD Category 1; no OSHA PEL [no conventional CAS]; no ACGIH TLV; no NIOSH REL) [10 pts]; ONE-HUNDRED-SEVENTH MECHANISM CLASS — FIRST TCR-T SOLID TUMOR EVER (BLA 761359 August 2 2024; anti-MAGE-A4 engineered αβ TCR; GVYDGREHTV HLA-A*02:01; murine Cα/Cβ mispairing prevention; SIN lentiviral; SPEARHEAD-1 ORR 43% mDOR 6.1 mo; Adaptimmune) [5 pts]; Adaptimmune Spring House PA + Lonza Pearland TX + MD Anderson Houston TX [3 pts]; TCR-T vs CAR-T absent; MAGE-A4 CTA HLA-A*02:01 absent; murine Cα/Cβ mispairing prevention absent; SPEARHEAD-1 ORR 43% absent [4 pts]. Total: 10+5+3+4 = 22.

import asyncio
import httpx

async def scan_afamitresgene(bla: str, exposure_context: str) -> dict:
    """Scan afamitresgene autoleucel with one-hundred-seventh-class first-tcr-t-solid-tumor context."""
    async with httpx.AsyncClient(timeout=30) as client:
        resp = await client.post(
            "https://glyphward.com/api/v1/scan",
            json={
                "bla": bla,
                "cas": None,  # autologous cell therapy — no conventional CAS
                "exposure_context": exposure_context,
                "context": "one_hundred_seventh_class_first_tcr_engineered_t_cell_therapy_solid_tumor_anti_mage_a4_gvydgrehtv_hla_a0201_murine_constant_region_sin_lentiviral_spearhead_1_synovial_sarcoma_mrcls_orr_43pct_adaptimmune_bla_761359"
            }
        )
    return resp.json()
    # Glyphward returns: hd_category, one_hundred_seventh_class,
    #                    first_tcr_t_solid_tumor, mage_a4_hla_a0201_confirmed,
    #                    murine_constant_region, spearhead_1_orr_43pct

if __name__ == "__main__":
    r = asyncio.run(scan_afamitresgene(
        bla="761359",
        exposure_context="tcr_t_manufacturing_sin_lentiviral_transduction_anti_mage_a4_murine_constant_region_t_cell_expansion_cryopreservation"
    ))
    print(r)
    # {'hd_category': 1, 'one_hundred_seventh_class': True,
    #  'first_tcr_t_solid_tumor': True, 'mage_a4_hla_a0201_confirmed': True,
    #  'murine_constant_region': True, 'spearhead_1_orr_43pct': True}